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Gabriella Torcia</h1><div class="affiliations-container fake-truncate js-profile-affiliations"><div><a class="u-tcGrayDarker" href="https://unifi.academia.edu/">Università degli Studi di Firenze (University of Florence)</a>, <a class="u-tcGrayDarker" href="https://unifi.academia.edu/Departments/Dept_of_Experimental_and_Clinical_Medicine/Documents">Dept of Experimental and Clinical Medicine</a>, <span class="u-tcGrayDarker">Faculty Member</span></div></div></div></div><div class="sidebar-cta-container"><button class="ds2-5-button hidden profile-cta-button grow js-profile-follow-button" data-broccoli-component="user-info.follow-button" data-click-track="profile-user-info-follow-button" data-follow-user-fname="Maria Gabriella" data-follow-user-id="32025990" data-follow-user-source="profile_button" data-has-google="false"><span class="material-symbols-outlined" style="font-size: 20px" translate="no">add</span>Follow</button><button class="ds2-5-button hidden profile-cta-button grow 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class="data">205</p></div></a><span><div class="stat-container"><p class="label"><span class="js-profile-total-view-text">Public Views</span></p><p class="data"><span class="js-profile-view-count"></span></p></div></span></div><div class="user-bio-container"><div class="profile-bio fake-truncate js-profile-about" style="margin: 0px;">Associate Professor in Microbiology and Clinical Microbiology (SSD MED/07) University of Firenze, School of Human Health Sciences, Department of Experimental and Clinical Medicine.<br />Teaching, Research and Clinical Activities.<br />PhD: General Hematology (Clinical and Laboratory).<br />Masters’ Degree in Medicine and Surgery.<br /><b>Address: </b>Department of Experimental and Clinical Medicine<br />University of Firenze<br />Viale Gaetano Pieraccini 6<br />I-50139<br />Firenze, Italy<br /><div class="js-profile-less-about u-linkUnstyled u-tcGrayDarker u-textDecorationUnderline u-displayNone">less</div></div></div><div class="ri-section"><div 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class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Maria Gabriella Torcia</h3></div><div class="js-work-strip profile--work_container" data-work-id="36060222"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060222/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases"><img alt="Research paper thumbnail of Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases" class="work-thumbnail" src="https://attachments.academia-assets.com/55945840/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060222/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases">Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/EPerissi">Eloisa Perissi</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. On the whole, our data suggest that the change in capsular phenotype may help bacterial cells of clade I to partially escape innate immune recognition and IL-1β-mediated inflammation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a2367482ea7035f0d7b7de7bf5f4a4f1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945840,"asset_id":36060222,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945840/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060222"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060222"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060222; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060222]").text(description); $(".js-view-count[data-work-id=36060222]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060222; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060222']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060222, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "a2367482ea7035f0d7b7de7bf5f4a4f1" } } $('.js-work-strip[data-work-id=36060222]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060222,"title":"Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases","translated_title":"","metadata":{"abstract":"ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060262"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060262/Effects_of_soluble_extracts_from_Leishmania_infantum_promastigotes_Toxoplasma_gondii_tachyzoites_on_TGF_b_mediated_pathways_in_activated_CD4_%C3%BE_T_lymphocytes"><img alt="Research paper thumbnail of Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes" class="work-thumbnail" src="https://attachments.academia-assets.com/55945878/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060262/Effects_of_soluble_extracts_from_Leishmania_infantum_promastigotes_Toxoplasma_gondii_tachyzoites_on_TGF_b_mediated_pathways_in_activated_CD4_%C3%BE_T_lymphocytes">Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/EPerissi">Eloisa Perissi</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Interference with transforming growth factor-b-mediated pathways helps several parasites to survi...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7b98a5f29cf66c0e2db5728cd782b57e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945878,"asset_id":36060262,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945878/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060262"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060262"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060262; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060262]").text(description); $(".js-view-count[data-work-id=36060262]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060262; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060262']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060262, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "7b98a5f29cf66c0e2db5728cd782b57e" } } $('.js-work-strip[data-work-id=36060262]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060262,"title":"Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes","translated_title":"","metadata":{"abstract":"Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells."},"translated_abstract":"Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059604"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059604/Bridging_pro_inflammatory_signals_synaptic_transmission_and_protection_in_spinal_explants_in_vitro"><img alt="Research paper thumbnail of Bridging pro-inflammatory signals, synaptic transmission and protection in spinal explants in vitro" class="work-thumbnail" src="https://attachments.academia-assets.com/55945115/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059604/Bridging_pro_inflammatory_signals_synaptic_transmission_and_protection_in_spinal_explants_in_vitro">Bridging pro-inflammatory signals, synaptic transmission and protection in spinal explants in vitro</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Multiple sclerosis is characterized by tissue atrophy involving the brain and the spinal cord, wh...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Multiple sclerosis is characterized by tissue atrophy involving the brain and the spinal cord, where reactive inflammation contributes to the neurodegenerative processes. Recently, the presence of synapse alterations induced by the inflammatory responses was suggested by experimental and clinical observations, in experimental autoimmune encephalomyelitis mouse model and in patients, respectively. Further knowledge on the interplay between pro-inflammatory agents, neuroglia and synaptic dysfunction is crucial to the design of unconventional protective molecules. Here we report the effects, on spinal cord circuits, of a cytokine cocktail that partly mimics the signature of T lymphocytes sub population Th1. In embryonic mouse spinal organ-cultures, containing neuronal cells and neuroglia, cytokines induced inflammatory responses accompanied by a significant increase in spontaneous synaptic activity. We suggest that cytokines specifically altered signal integration in spinal networks by speeding the decay of GABA A responses. This hypothesis is supported by the finding that synapse protection by a non-peptidic NGF mimetic molecule prevented both the changes in the time course of GABA events and in network activity that were left unchanged by the cytokine production from astrocytes and microglia present in the cultured tissue. In conclusion, we developed an important tool for the study of synaptic alterations induced by inflammation, that takes into account the role of neuronal and not neuronal resident cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="20cff893dd9ed9c1cfb98c741df5da00" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945115,"asset_id":36059604,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945115/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059604"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059604"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059604; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059604]").text(description); $(".js-view-count[data-work-id=36059604]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059604; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059604']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059604, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "20cff893dd9ed9c1cfb98c741df5da00" } } $('.js-work-strip[data-work-id=36059604]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059604,"title":"Bridging pro-inflammatory signals, synaptic transmission and protection in spinal explants in vitro","translated_title":"","metadata":{"abstract":"Multiple sclerosis is characterized by tissue atrophy involving the brain and the spinal cord, where reactive inflammation contributes to the neurodegenerative processes. Recently, the presence of synapse alterations induced by the inflammatory responses was suggested by experimental and clinical observations, in experimental autoimmune encephalomyelitis mouse model and in patients, respectively. Further knowledge on the interplay between pro-inflammatory agents, neuroglia and synaptic dysfunction is crucial to the design of unconventional protective molecules. Here we report the effects, on spinal cord circuits, of a cytokine cocktail that partly mimics the signature of T lymphocytes sub population Th1. In embryonic mouse spinal organ-cultures, containing neuronal cells and neuroglia, cytokines induced inflammatory responses accompanied by a significant increase in spontaneous synaptic activity. We suggest that cytokines specifically altered signal integration in spinal networks by speeding the decay of GABA A responses. This hypothesis is supported by the finding that synapse protection by a non-peptidic NGF mimetic molecule prevented both the changes in the time course of GABA events and in network activity that were left unchanged by the cytokine production from astrocytes and microglia present in the cultured tissue. In conclusion, we developed an important tool for the study of synaptic alterations induced by inflammation, that takes into account the role of neuronal and not neuronal resident cells."},"translated_abstract":"Multiple sclerosis is characterized by tissue atrophy involving the brain and the spinal cord, where reactive inflammation contributes to the neurodegenerative processes. Recently, the presence of synapse alterations induced by the inflammatory responses was suggested by experimental and clinical observations, in experimental autoimmune encephalomyelitis mouse model and in patients, respectively. Further knowledge on the interplay between pro-inflammatory agents, neuroglia and synaptic dysfunction is crucial to the design of unconventional protective molecules. Here we report the effects, on spinal cord circuits, of a cytokine cocktail that partly mimics the signature of T lymphocytes sub population Th1. In embryonic mouse spinal organ-cultures, containing neuronal cells and neuroglia, cytokines induced inflammatory responses accompanied by a significant increase in spontaneous synaptic activity. We suggest that cytokines specifically altered signal integration in spinal networks by speeding the decay of GABA A responses. This hypothesis is supported by the finding that synapse protection by a non-peptidic NGF mimetic molecule prevented both the changes in the time course of GABA events and in network activity that were left unchanged by the cytokine production from astrocytes and microglia present in the cultured tissue. In conclusion, we developed an important tool for the study of synaptic alterations induced by inflammation, that takes into account the role of neuronal and not neuronal resident cells.","internal_url":"https://www.academia.edu/36059604/Bridging_pro_inflammatory_signals_synaptic_transmission_and_protection_in_spinal_explants_in_vitro","translated_internal_url":"","created_at":"2018-03-02T05:36:28.613-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136561,"work_id":36059604,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Bridging pro-inflammatory signals, synaptic transmission and protection in spinal explants in vitro"}],"downloadable_attachments":[{"id":55945115,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945115/thumbnails/1.jpg","file_name":"Bridging_pro-inflammatory_signals__synaptic.pdf","download_url":"https://www.academia.edu/attachments/55945115/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Bridging_pro_inflammatory_signals_synapt.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945115/Bridging_pro-inflammatory_signals__synaptic-libre.pdf?1519998791=\u0026response-content-disposition=attachment%3B+filename%3DBridging_pro_inflammatory_signals_synapt.pdf\u0026Expires=1732404749\u0026Signature=V04KAfctg9seCaQHBxk-2SCRfxxMATnK3FLhXtWIkdDu9vKYw4llYtXH2YAkpYcaR~R~Eg1K7h53zV3Z069g-PHNccwLObBLlQs0jHZyEZIF9iv~sRRzOPEG59rcD5SdrQ984V3Mu2nUEDjqXskvRzX-OmlKw2bC9WHn5Qb1ZbYtLXI2b9AxNhXqzpUXhCqXW9HP45MQ2Nv1wNl4YaCfZOkdgmBu2B7EaCdHApbk~9jKxPA5VWvTyYUPf3asFR3Sa8m0cRtAxrcD2wXWHadUIgXPbBGIuA4qxPdgEMJMWKldG4SObI0qu2dti5F6xrjP-vein9kuFlY4mpp3Pwrcjw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Bridging_pro_inflammatory_signals_synaptic_transmission_and_protection_in_spinal_explants_in_vitro","translated_slug":"","page_count":14,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945115,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945115/thumbnails/1.jpg","file_name":"Bridging_pro-inflammatory_signals__synaptic.pdf","download_url":"https://www.academia.edu/attachments/55945115/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Bridging_pro_inflammatory_signals_synapt.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945115/Bridging_pro-inflammatory_signals__synaptic-libre.pdf?1519998791=\u0026response-content-disposition=attachment%3B+filename%3DBridging_pro_inflammatory_signals_synapt.pdf\u0026Expires=1732404749\u0026Signature=V04KAfctg9seCaQHBxk-2SCRfxxMATnK3FLhXtWIkdDu9vKYw4llYtXH2YAkpYcaR~R~Eg1K7h53zV3Z069g-PHNccwLObBLlQs0jHZyEZIF9iv~sRRzOPEG59rcD5SdrQ984V3Mu2nUEDjqXskvRzX-OmlKw2bC9WHn5Qb1ZbYtLXI2b9AxNhXqzpUXhCqXW9HP45MQ2Nv1wNl4YaCfZOkdgmBu2B7EaCdHApbk~9jKxPA5VWvTyYUPf3asFR3Sa8m0cRtAxrcD2wXWHadUIgXPbBGIuA4qxPdgEMJMWKldG4SObI0qu2dti5F6xrjP-vein9kuFlY4mpp3Pwrcjw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":3097,"name":"Multiple sclerosis","url":"https://www.academia.edu/Documents/in/Multiple_sclerosis"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059619"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059619/Characterization_of_cervico_vaginal_microbiota_in_women_developing_persistent_high_risk_Human_Papillomavirus_infection"><img alt="Research paper thumbnail of Characterization of cervico-vaginal microbiota in women developing persistent high-risk Human Papillomavirus infection" class="work-thumbnail" src="https://attachments.academia-assets.com/55945126/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059619/Characterization_of_cervico_vaginal_microbiota_in_women_developing_persistent_high_risk_Human_Papillomavirus_infection">Characterization of cervico-vaginal microbiota in women developing persistent high-risk Human Papillomavirus infection</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Changes in cervico-vaginal microbiota with Lactobacillus depletion and increased microbial divers...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Changes in cervico-vaginal microbiota with Lactobacillus depletion and increased microbial diversity facilitate human papillomavirus (HPV) infection and might be involved in viral persistence and cancer development. To define the microbial Community State Types (CSTs) associated with high-risk HPV− persistence, we analysed 55 cervico-vaginal samples from HPV positive (HPV+) women out of 1029 screened women and performed pyrosequencing of 16S rDNA. A total of 17 samples from age-matched HPV negative (HPV−) women were used as control. Clearance or Persistence groups were defined by recalling women after one year for HPV screening and genotyping. A CST IV subgroup, with bacterial genera such as Gardnerella, Prevotella, Megasphoera, Atopobium, frequently associated with anaerobic consortium in bacterial vaginosis (BV), was present at baseline sampling in 43% of women in Persistence group, and only in 7.4% of women in Clearance group. Atopobium genus was significantly enriched in Persistence group compared to the other groups. Sialidase-encoding gene from Gardnerella vaginalis, involved in biofilm formation, was significantly more represented in Persistence group compared to the other groups. Based on these data, we consider the CST IV-BV as a risk factor for HPV persistence and we propose Atopobium spp and sialidase gene from G. vaginalis as microbial markers of HPV− persistence. Cervical cancer (CC) is one of the most common cancer in women, with an estimated incidence of 485 000 new cases and 236 000 deaths in 2013 1 , causing 6.9 million disability-adjusted life-years (DALYs). Persistence of onco-genic human papillomavirus (HPV) infection contribute to the development of CC. While the virus is cleared in more than 90% of infections within 6–18 months 2–4 , viral persistence occurs in almost 10% of infected women. The factors responsible of persistence, as well those that promote and initiate the carcinogenesis process, need to be fully elucidated. Many other factors such as immunodeficiency, age, smoking, oral contraceptives and Chlamydia trachomatis infection are related with higher persistence rates 5, 6. Recently, several scientific reports indicated the role of vaginal microbiota in the acquisition and persistence of HPV and risk of CC development 7. In the majority of human body sites, highly diverse microbial communities are generally considered a signature of health 8, 9. However, in the vaginal environment, health is commonly associated with low microbial diversity and prevalence of only a few species of Lactobacillus 10–13. Lactobacillus spp. prevent colonization of exogenous pathogens by producing lactic acid, bacteriocins and reactive oxygen species (ROS), and compete with them for Published: xx xx xxxx OPEN</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f93e76508674e5161bfc9aca846be6c4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945126,"asset_id":36059619,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945126/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059619"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059619"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059619; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059619]").text(description); $(".js-view-count[data-work-id=36059619]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059619; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059619']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059619, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "f93e76508674e5161bfc9aca846be6c4" } } $('.js-work-strip[data-work-id=36059619]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059619,"title":"Characterization of cervico-vaginal microbiota in women developing persistent high-risk Human Papillomavirus infection","translated_title":"","metadata":{"abstract":"Changes in cervico-vaginal microbiota with Lactobacillus depletion and increased microbial diversity facilitate human papillomavirus (HPV) infection and might be involved in viral persistence and cancer development. To define the microbial Community State Types (CSTs) associated with high-risk HPV− persistence, we analysed 55 cervico-vaginal samples from HPV positive (HPV+) women out of 1029 screened women and performed pyrosequencing of 16S rDNA. A total of 17 samples from age-matched HPV negative (HPV−) women were used as control. Clearance or Persistence groups were defined by recalling women after one year for HPV screening and genotyping. A CST IV subgroup, with bacterial genera such as Gardnerella, Prevotella, Megasphoera, Atopobium, frequently associated with anaerobic consortium in bacterial vaginosis (BV), was present at baseline sampling in 43% of women in Persistence group, and only in 7.4% of women in Clearance group. Atopobium genus was significantly enriched in Persistence group compared to the other groups. Sialidase-encoding gene from Gardnerella vaginalis, involved in biofilm formation, was significantly more represented in Persistence group compared to the other groups. Based on these data, we consider the CST IV-BV as a risk factor for HPV persistence and we propose Atopobium spp and sialidase gene from G. vaginalis as microbial markers of HPV− persistence. Cervical cancer (CC) is one of the most common cancer in women, with an estimated incidence of 485 000 new cases and 236 000 deaths in 2013 1 , causing 6.9 million disability-adjusted life-years (DALYs). Persistence of onco-genic human papillomavirus (HPV) infection contribute to the development of CC. While the virus is cleared in more than 90% of infections within 6–18 months 2–4 , viral persistence occurs in almost 10% of infected women. The factors responsible of persistence, as well those that promote and initiate the carcinogenesis process, need to be fully elucidated. Many other factors such as immunodeficiency, age, smoking, oral contraceptives and Chlamydia trachomatis infection are related with higher persistence rates 5, 6. Recently, several scientific reports indicated the role of vaginal microbiota in the acquisition and persistence of HPV and risk of CC development 7. In the majority of human body sites, highly diverse microbial communities are generally considered a signature of health 8, 9. However, in the vaginal environment, health is commonly associated with low microbial diversity and prevalence of only a few species of Lactobacillus 10–13. Lactobacillus spp. prevent colonization of exogenous pathogens by producing lactic acid, bacteriocins and reactive oxygen species (ROS), and compete with them for Published: xx xx xxxx OPEN"},"translated_abstract":"Changes in cervico-vaginal microbiota with Lactobacillus depletion and increased microbial diversity facilitate human papillomavirus (HPV) infection and might be involved in viral persistence and cancer development. To define the microbial Community State Types (CSTs) associated with high-risk HPV− persistence, we analysed 55 cervico-vaginal samples from HPV positive (HPV+) women out of 1029 screened women and performed pyrosequencing of 16S rDNA. A total of 17 samples from age-matched HPV negative (HPV−) women were used as control. Clearance or Persistence groups were defined by recalling women after one year for HPV screening and genotyping. A CST IV subgroup, with bacterial genera such as Gardnerella, Prevotella, Megasphoera, Atopobium, frequently associated with anaerobic consortium in bacterial vaginosis (BV), was present at baseline sampling in 43% of women in Persistence group, and only in 7.4% of women in Clearance group. Atopobium genus was significantly enriched in Persistence group compared to the other groups. Sialidase-encoding gene from Gardnerella vaginalis, involved in biofilm formation, was significantly more represented in Persistence group compared to the other groups. Based on these data, we consider the CST IV-BV as a risk factor for HPV persistence and we propose Atopobium spp and sialidase gene from G. vaginalis as microbial markers of HPV− persistence. Cervical cancer (CC) is one of the most common cancer in women, with an estimated incidence of 485 000 new cases and 236 000 deaths in 2013 1 , causing 6.9 million disability-adjusted life-years (DALYs). Persistence of onco-genic human papillomavirus (HPV) infection contribute to the development of CC. While the virus is cleared in more than 90% of infections within 6–18 months 2–4 , viral persistence occurs in almost 10% of infected women. The factors responsible of persistence, as well those that promote and initiate the carcinogenesis process, need to be fully elucidated. Many other factors such as immunodeficiency, age, smoking, oral contraceptives and Chlamydia trachomatis infection are related with higher persistence rates 5, 6. Recently, several scientific reports indicated the role of vaginal microbiota in the acquisition and persistence of HPV and risk of CC development 7. In the majority of human body sites, highly diverse microbial communities are generally considered a signature of health 8, 9. However, in the vaginal environment, health is commonly associated with low microbial diversity and prevalence of only a few species of Lactobacillus 10–13. Lactobacillus spp. prevent colonization of exogenous pathogens by producing lactic acid, bacteriocins and reactive oxygen species (ROS), and compete with them for Published: xx xx xxxx OPEN","internal_url":"https://www.academia.edu/36059619/Characterization_of_cervico_vaginal_microbiota_in_women_developing_persistent_high_risk_Human_Papillomavirus_infection","translated_internal_url":"","created_at":"2018-03-02T05:38:19.144-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136565,"work_id":36059619,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Characterization of cervico-vaginal microbiota in women developing persistent high-risk Human Papillomavirus infection"}],"downloadable_attachments":[{"id":55945126,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945126/thumbnails/1.jpg","file_name":"Characterization_of_cervico-vaginal_microbiota_in_women_developing_persistent_high-risk_Human_Papillomavirus_infection.pdf","download_url":"https://www.academia.edu/attachments/55945126/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Characterization_of_cervico_vaginal_micr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945126/Characterization_of_cervico-vaginal_microbiota_in_women_developing_persistent_high-risk_Human_Papillomavirus_infection-libre.pdf?1519998785=\u0026response-content-disposition=attachment%3B+filename%3DCharacterization_of_cervico_vaginal_micr.pdf\u0026Expires=1732263172\u0026Signature=K7O-HPlJWnOkMcGtvMqQDJtGTXwxU2QOSFohQX7~X2GM5wnnsOHrNzxWp00a5cpZIdJfKgoW6yl4WTY0~oAYVh~n13MKW4lu~42SlJZxs6CD9BcfVPKE8i-ZzBnAZF01ywWxfJa5-yIe2uPrXih0YuCAq9jCb-qCeao~TdwH~3gcie9fIvdCp8Ze1g7djmLGmyttF4MrRb8JEED~Gxxva83qmtKKsNIChCLascr4RCZV6bTpuuys1rGrRcdaIRAvvzYMLip03IhFrjYo6LXWvh~FwqEGWTs8xx6qxrsyYKpw-DiIbgn6WBXtzD1heTTrlGq~h8mFVlbaMWBzoQ1V9A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Characterization_of_cervico_vaginal_microbiota_in_women_developing_persistent_high_risk_Human_Papillomavirus_infection","translated_slug":"","page_count":12,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945126,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945126/thumbnails/1.jpg","file_name":"Characterization_of_cervico-vaginal_microbiota_in_women_developing_persistent_high-risk_Human_Papillomavirus_infection.pdf","download_url":"https://www.academia.edu/attachments/55945126/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Characterization_of_cervico_vaginal_micr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945126/Characterization_of_cervico-vaginal_microbiota_in_women_developing_persistent_high-risk_Human_Papillomavirus_infection-libre.pdf?1519998785=\u0026response-content-disposition=attachment%3B+filename%3DCharacterization_of_cervico_vaginal_micr.pdf\u0026Expires=1732263172\u0026Signature=K7O-HPlJWnOkMcGtvMqQDJtGTXwxU2QOSFohQX7~X2GM5wnnsOHrNzxWp00a5cpZIdJfKgoW6yl4WTY0~oAYVh~n13MKW4lu~42SlJZxs6CD9BcfVPKE8i-ZzBnAZF01ywWxfJa5-yIe2uPrXih0YuCAq9jCb-qCeao~TdwH~3gcie9fIvdCp8Ze1g7djmLGmyttF4MrRb8JEED~Gxxva83qmtKKsNIChCLascr4RCZV6bTpuuys1rGrRcdaIRAvvzYMLip03IhFrjYo6LXWvh~FwqEGWTs8xx6qxrsyYKpw-DiIbgn6WBXtzD1heTTrlGq~h8mFVlbaMWBzoQ1V9A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":173523,"name":"HPV","url":"https://www.academia.edu/Documents/in/HPV"},{"id":203512,"name":"Cervical Cancer","url":"https://www.academia.edu/Documents/in/Cervical_Cancer"},{"id":465741,"name":"Vaginal Microbiota","url":"https://www.academia.edu/Documents/in/Vaginal_Microbiota"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059652"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059652/Differential_Th17_response_induced_by_the_two_clades_of_the_pandemic_ST258_Klebsiella_pneumoniae_clonal_lineages_producing_KPC_type_carbapenemase"><img alt="Research paper thumbnail of Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC- type carbapenemase" class="work-thumbnail" src="https://attachments.academia-assets.com/55945151/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059652/Differential_Th17_response_induced_by_the_two_clades_of_the_pandemic_ST258_Klebsiella_pneumoniae_clonal_lineages_producing_KPC_type_carbapenemase">Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC- type carbapenemase</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The spread of KPC-type carbapenemases is mainly attributed to the global dissemination of Klebsie...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The spread of KPC-type carbapenemases is mainly attributed to the global dissemination of Klebsiella pneumoniae (KP) strains belonging to the clonal group (CG) 258, including sequence type (ST) 258 and other related STs. Two distinct clades of CG258-KP have evolved, which differ mainly for the composition of their capsular polysaccharides, and recent studies indicate that clade 1 evolved from an ancestor of clade 2 by recombination of a genomic fragment carrying the capsular polysaccharide (cps) locus. In this paper, we investigated the ability of two ST258-KP strains, KKBO-1 and KK207-1, selected as representatives of ST258-KP clade 2 and clade 1, respectively, to activate an adaptive immune response using ex vivo-stimulation of PBMC from normal donors as an experimental model. Our data showed that KKBO-1 (clade 2) induces a Th17 response more efficiently than KK207-1 (clade 1): the percentage of CD4 + IL17 + cells and the production of IL-17A were significantly higher in cultures with KKBO-1 compared to cultures with KK207-1. While no differences in the rate of bacterial internalization or in the bacteria-induced expression of CD86 and HLA-DR by monocytes and myeloid dendritic cells were revealed, we found that the two strains significantly differ in inducing the production of cytokines involved in the adaptive immune response, as IL-1β, IL-23 and TNF-α, by antigen-presenting cells, with KKBO-1 being a more efficient inducer than KK207-1. The immune responses elicited by KK207-1 were comparable to those elicited by CIP 52.145, a highly virulent K. pneumoniae reference strain known to escape immune-inflammatory responses. Altogether, present results suggest that CG258-KP of the two clades are capable of inducing a different response of adaptive immunity in the human host.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="778924d6aa0552240b3936bccd481a18" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945151,"asset_id":36059652,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945151/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059652"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059652"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059652; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059652]").text(description); $(".js-view-count[data-work-id=36059652]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059652; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059652']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059652, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "778924d6aa0552240b3936bccd481a18" } } $('.js-work-strip[data-work-id=36059652]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059652,"title":"Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC- type carbapenemase","translated_title":"","metadata":{"abstract":"The spread of KPC-type carbapenemases is mainly attributed to the global dissemination of Klebsiella pneumoniae (KP) strains belonging to the clonal group (CG) 258, including sequence type (ST) 258 and other related STs. 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Our data showed that KKBO-1 (clade 2) induces a Th17 response more efficiently than KK207-1 (clade 1): the percentage of CD4 + IL17 + cells and the production of IL-17A were significantly higher in cultures with KKBO-1 compared to cultures with KK207-1. While no differences in the rate of bacterial internalization or in the bacteria-induced expression of CD86 and HLA-DR by monocytes and myeloid dendritic cells were revealed, we found that the two strains significantly differ in inducing the production of cytokines involved in the adaptive immune response, as IL-1β, IL-23 and TNF-α, by antigen-presenting cells, with KKBO-1 being a more efficient inducer than KK207-1. The immune responses elicited by KK207-1 were comparable to those elicited by CIP 52.145, a highly virulent K. pneumoniae reference strain known to escape immune-inflammatory responses. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059681"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059681/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes"><img alt="Research paper thumbnail of Crohn's Colitis: Development of a multiplex gene expression assay comparing mRNA levels of susceptibility genes" class="work-thumbnail" src="https://attachments.academia-assets.com/55945201/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059681/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes">Crohn's Colitis: Development of a multiplex gene expression assay comparing mRNA levels of susceptibility genes</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Crohn's disease (CD) is a multifactorial immunologically mediated disease. In this study we explo...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Crohn's disease (CD) is a multifactorial immunologically mediated disease. In this study we explored, for the first time, the efficacy of the Multiplex Gene Assay technology for detecting mRNA expression profile of 24 selected CD related genes in endoscopic biopsies and surgical specimens from CD patients with colonic localization of the disease. The polymorphisms of genes most frequently associated with CD were also analysed in DNA samples from the same patients. The analysis of endoscopic samples showed increased expression of 7 genes in inflamed mucosa compared to non-inflamed mucosa and suggests the activation of the autophagy process and of a Th17 adaptive response. The analysis of surgical specimens showed increased expression of 16 genes in inflamed tissue compared to non-inflamed internal controls and revealed the activation of immune-adaptive Th17 response in association with a Th1 response.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="98d3596305eca6fb3ce932edcb230d7b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945201,"asset_id":36059681,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945201/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059681"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059681"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059681; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059681]").text(description); $(".js-view-count[data-work-id=36059681]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059681; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059681']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059681, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "98d3596305eca6fb3ce932edcb230d7b" } } $('.js-work-strip[data-work-id=36059681]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059681,"title":"Crohn's Colitis: Development of a multiplex gene expression assay comparing mRNA levels of susceptibility genes","translated_title":"","metadata":{"abstract":"Crohn's disease (CD) is a multifactorial immunologically mediated disease. In this study we explored, for the first time, the efficacy of the Multiplex Gene Assay technology for detecting mRNA expression profile of 24 selected CD related genes in endoscopic biopsies and surgical specimens from CD patients with colonic localization of the disease. The polymorphisms of genes most frequently associated with CD were also analysed in DNA samples from the same patients. The analysis of endoscopic samples showed increased expression of 7 genes in inflamed mucosa compared to non-inflamed mucosa and suggests the activation of the autophagy process and of a Th17 adaptive response. The analysis of surgical specimens showed increased expression of 16 genes in inflamed tissue compared to non-inflamed internal controls and revealed the activation of immune-adaptive Th17 response in association with a Th1 response."},"translated_abstract":"Crohn's disease (CD) is a multifactorial immunologically mediated disease. In this study we explored, for the first time, the efficacy of the Multiplex Gene Assay technology for detecting mRNA expression profile of 24 selected CD related genes in endoscopic biopsies and surgical specimens from CD patients with colonic localization of the disease. The polymorphisms of genes most frequently associated with CD were also analysed in DNA samples from the same patients. The analysis of endoscopic samples showed increased expression of 7 genes in inflamed mucosa compared to non-inflamed mucosa and suggests the activation of the autophagy process and of a Th17 adaptive response. The analysis of surgical specimens showed increased expression of 16 genes in inflamed tissue compared to non-inflamed internal controls and revealed the activation of immune-adaptive Th17 response in association with a Th1 response.","internal_url":"https://www.academia.edu/36059681/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes","translated_internal_url":"","created_at":"2018-03-02T05:47:27.816-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":55945201,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945201/thumbnails/1.jpg","file_name":"Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes.pdf","download_url":"https://www.academia.edu/attachments/55945201/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Crohns_Colitis_Development_of_a_multiple.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945201/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes-libre.pdf?1519999050=\u0026response-content-disposition=attachment%3B+filename%3DCrohns_Colitis_Development_of_a_multiple.pdf\u0026Expires=1732404749\u0026Signature=T7M7KtkGUz9dwQOLbAqZibvoXVHb6vQA-ae4-WRAVv0DL3saxjPVVKV~uuyjVfkVIuBBLARnYRfT8r1nxqObP9La-NImYOFtMAS0UJfRmAg9jQIUN8JZ64AYXZiVtmWsj25BJDtyp0qFocAAmPOiRLTt0XJT9efQx0Ib7j9Yi7BdVm22qYP39vEkGD79hMrNwSsSNNbPL-1UZDACaSmHhs1VCMCYh4YCvx3TLaVJZ0euRsVhEQpbvmPvNJcjsdRo71XRTR7vFFDxfwuTVP3bCm0ayjttsIKXz50TkItmxzwhOfroE5pplgSNBMk9yfQsCf1w6-KWp9y0tMmtHXawuw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes","translated_slug":"","page_count":10,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945201,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945201/thumbnails/1.jpg","file_name":"Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes.pdf","download_url":"https://www.academia.edu/attachments/55945201/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Crohns_Colitis_Development_of_a_multiple.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945201/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes-libre.pdf?1519999050=\u0026response-content-disposition=attachment%3B+filename%3DCrohns_Colitis_Development_of_a_multiple.pdf\u0026Expires=1732404749\u0026Signature=T7M7KtkGUz9dwQOLbAqZibvoXVHb6vQA-ae4-WRAVv0DL3saxjPVVKV~uuyjVfkVIuBBLARnYRfT8r1nxqObP9La-NImYOFtMAS0UJfRmAg9jQIUN8JZ64AYXZiVtmWsj25BJDtyp0qFocAAmPOiRLTt0XJT9efQx0Ib7j9Yi7BdVm22qYP39vEkGD79hMrNwSsSNNbPL-1UZDACaSmHhs1VCMCYh4YCvx3TLaVJZ0euRsVhEQpbvmPvNJcjsdRo71XRTR7vFFDxfwuTVP3bCm0ayjttsIKXz50TkItmxzwhOfroE5pplgSNBMk9yfQsCf1w6-KWp9y0tMmtHXawuw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":59365,"name":"Crohn's Disease","url":"https://www.academia.edu/Documents/in/Crohns_Disease"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059703"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059703/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases"><img alt="Research paper thumbnail of Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases" class="work-thumbnail" src="https://attachments.academia-assets.com/55945221/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059703/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases">Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. On the whole, our data suggest that the change in capsular phenotype may help bacterial cells of clade I to partially escape innate immune recognition and IL-1β-mediated inflammation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="34d0c3b69a38a4d045fdbd42a9268c48" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945221,"asset_id":36059703,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945221/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059703"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059703"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059703; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059703]").text(description); $(".js-view-count[data-work-id=36059703]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059703; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059703']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059703, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "34d0c3b69a38a4d045fdbd42a9268c48" } } $('.js-work-strip[data-work-id=36059703]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059703,"title":"Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases","translated_title":"","metadata":{"abstract":"ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. On the whole, our data suggest that the change in capsular phenotype may help bacterial cells of clade I to partially escape innate immune recognition and IL-1β-mediated inflammation."},"translated_abstract":"ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. On the whole, our data suggest that the change in capsular phenotype may help bacterial cells of clade I to partially escape innate immune recognition and IL-1β-mediated inflammation.","internal_url":"https://www.academia.edu/36059703/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases","translated_internal_url":"","created_at":"2018-03-02T05:50:46.939-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136591,"work_id":36059703,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases"},{"id":31136592,"work_id":36059703,"tagging_user_id":32025990,"tagged_user_id":32099627,"co_author_invite_id":null,"email":"m***i@unifi.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":2,"name":"Michele Tanturli","title":"Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases"}],"downloadable_attachments":[{"id":55945221,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945221/thumbnails/1.jpg","file_name":"Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae.pdf","download_url":"https://www.academia.edu/attachments/55945221/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Differences_in_Inflammatory_Response_Ind.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945221/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae-libre.pdf?1519999383=\u0026response-content-disposition=attachment%3B+filename%3DDifferences_in_Inflammatory_Response_Ind.pdf\u0026Expires=1732404749\u0026Signature=Mnnka6KY~fdtrzUL6sGwhMuFrlgWD5jrFc22Xg2PeWoa7qCbSlNSgVT5joHlramMuNFpcirJ1BTK65IrwKLr1c3XPxu0ul08q2h9TYkkpCkcF6hCAspFws6GKSTDWoEiBCkfuktKr03u5dlrS55kibKKd58SaOFpl8GCrl1bpEX2dPvE8rR8VyhERlLxrXzWnNwGO4ZRrTV2RFQL7V5KzbE5PiVy~f2mZ6yibhJ4c1NUEioX9yZhYYihLy0ZxMNAAJLoRDCjDGjSFecDcBXwUmFEBDPvtanDfV-hFNVa~UaNMsGjuWiF4IFyIBRHgcrG3x0t3HqepMv6I~QoMx4GUQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases","translated_slug":"","page_count":17,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945221,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945221/thumbnails/1.jpg","file_name":"Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae.pdf","download_url":"https://www.academia.edu/attachments/55945221/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Differences_in_Inflammatory_Response_Ind.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945221/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae-libre.pdf?1519999383=\u0026response-content-disposition=attachment%3B+filename%3DDifferences_in_Inflammatory_Response_Ind.pdf\u0026Expires=1732404749\u0026Signature=Mnnka6KY~fdtrzUL6sGwhMuFrlgWD5jrFc22Xg2PeWoa7qCbSlNSgVT5joHlramMuNFpcirJ1BTK65IrwKLr1c3XPxu0ul08q2h9TYkkpCkcF6hCAspFws6GKSTDWoEiBCkfuktKr03u5dlrS55kibKKd58SaOFpl8GCrl1bpEX2dPvE8rR8VyhERlLxrXzWnNwGO4ZRrTV2RFQL7V5KzbE5PiVy~f2mZ6yibhJ4c1NUEioX9yZhYYihLy0ZxMNAAJLoRDCjDGjSFecDcBXwUmFEBDPvtanDfV-hFNVa~UaNMsGjuWiF4IFyIBRHgcrG3x0t3HqepMv6I~QoMx4GUQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":112322,"name":"Klebsiella","url":"https://www.academia.edu/Documents/in/Klebsiella"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="16117323"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/16117323/Effects_of_near_infrared_laser_radiation_on_the_survival_and_inflammatory_potential_of_Candida_spp_involved_in_the_pathogenesis_of_chemotherapy_induced_oral_mucositis"><img alt="Research paper thumbnail of Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/16117323/Effects_of_near_infrared_laser_radiation_on_the_survival_and_inflammatory_potential_of_Candida_spp_involved_in_the_pathogenesis_of_chemotherapy_induced_oral_mucositis">Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MicheleTanturli">Michele Tanturli</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/LisaRizzetto">Lisa Rizzetto</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Candida spp. usually colonize ulcerative lesions of atrophic mucosa in patients with chemotherapy...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Candida spp. usually colonize ulcerative lesions of atrophic mucosa in patients with chemotherapy-induced oral mucositis inducing severe inflammation. The spread of antifungal-esistant strains strongly encouraged the search of complementary or alternative therapeutic strategies to cure inflamed mucosa. In this paper, we studied the effects of a near-infrared (NIR) laser system with dual-wavelength emission (808 nm+904 nm) on the survival and inflammatory potential of C. albicans, C. glabrata, and C. parapsilosis. Laser treatment was performed with a Multiwave Locked System laser. Survival and apoptosis of fungal strains were evaluated by colony-forming units (CFU)  counting and annexin V staining. Cytokine production was evaluated by ImmunoPlex array. Laser treatment significantly affected the survival of Candida spp. by inducing apoptosis and  induced a lower production of inflammatory cytokines by dendritic cells compared to untreated fungi. No differences in the survival and inflammatory potential were recorded in treated or untreated Saccharomyces cerevisiae cells, used as the control nonpathogenic microorganism. Laser treatment altered the survival and inflammatory potential of pathogenic Candida spp. These data provide experimental support to the use of NIR laser radiation as a co-adjuvant of antifungal therapy in patients with oral mucositis (OM) complicated by Candida infections.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="16117323"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="16117323"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 16117323; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=16117323]").text(description); $(".js-view-count[data-work-id=16117323]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 16117323; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='16117323']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 16117323, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=16117323]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":16117323,"title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis","translated_title":"","metadata":{"abstract":"Candida spp. usually colonize ulcerative lesions of atrophic mucosa in patients with chemotherapy-induced oral mucositis inducing severe inflammation. The spread of antifungal-esistant strains strongly encouraged the search of complementary or alternative therapeutic strategies to cure inflamed mucosa. In this paper, we studied the effects of a near-infrared (NIR) laser system with dual-wavelength emission (808 nm+904 nm) on the survival and inflammatory potential of C. albicans, C. glabrata, and C. parapsilosis. Laser treatment was performed with a Multiwave Locked System laser. Survival and apoptosis of fungal strains were evaluated by colony-forming units (CFU) counting and annexin V staining. Cytokine production was evaluated by ImmunoPlex array. Laser treatment significantly affected the survival of Candida spp. by inducing apoptosis and induced a lower production of inflammatory cytokines by dendritic cells compared to untreated fungi. No differences in the survival and inflammatory potential were recorded in treated or untreated Saccharomyces cerevisiae cells, used as the control nonpathogenic microorganism. Laser treatment altered the survival and inflammatory potential of pathogenic Candida spp. These data provide experimental support to the use of NIR laser radiation as a co-adjuvant of antifungal therapy in patients with oral mucositis (OM) complicated by Candida infections."},"translated_abstract":"Candida spp. usually colonize ulcerative lesions of atrophic mucosa in patients with chemotherapy-induced oral mucositis inducing severe inflammation. The spread of antifungal-esistant strains strongly encouraged the search of complementary or alternative therapeutic strategies to cure inflamed mucosa. In this paper, we studied the effects of a near-infrared (NIR) laser system with dual-wavelength emission (808 nm+904 nm) on the survival and inflammatory potential of C. albicans, C. glabrata, and C. parapsilosis. Laser treatment was performed with a Multiwave Locked System laser. Survival and apoptosis of fungal strains were evaluated by colony-forming units (CFU) counting and annexin V staining. Cytokine production was evaluated by ImmunoPlex array. Laser treatment significantly affected the survival of Candida spp. by inducing apoptosis and induced a lower production of inflammatory cytokines by dendritic cells compared to untreated fungi. No differences in the survival and inflammatory potential were recorded in treated or untreated Saccharomyces cerevisiae cells, used as the control nonpathogenic microorganism. Laser treatment altered the survival and inflammatory potential of pathogenic Candida spp. These data provide experimental support to the use of NIR laser radiation as a co-adjuvant of antifungal therapy in patients with oral mucositis (OM) complicated by Candida infections.","internal_url":"https://www.academia.edu/16117323/Effects_of_near_infrared_laser_radiation_on_the_survival_and_inflammatory_potential_of_Candida_spp_involved_in_the_pathogenesis_of_chemotherapy_induced_oral_mucositis","translated_internal_url":"","created_at":"2015-09-24T01:58:59.945-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32099627,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":6209098,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":32097049,"co_author_invite_id":null,"email":"a***e@virgilio.it","display_order":0,"name":"Annmaria Clemente","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209099,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":31719145,"co_author_invite_id":null,"email":"l***o@fmach.it","display_order":4194304,"name":"Lisa Rizzetto","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209100,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":14476117,"co_author_invite_id":null,"email":"m***w@email.it","display_order":6291456,"name":"Eloisa Perissi","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209101,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":7340032,"name":"Federico Cozzolino","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209102,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":22224088,"co_author_invite_id":null,"email":"f***i@libero.it","display_order":7864320,"name":"Franco Fusi","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209103,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":3382639,"co_author_invite_id":null,"email":"v***o@yahoo.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":8126464,"name":"Leonardo Vignali","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":25071196,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":32025990,"co_author_invite_id":null,"email":"m***a@unifi.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":8323072,"name":"Maria Gabriella Torcia","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"}],"downloadable_attachments":[],"slug":"Effects_of_near_infrared_laser_radiation_on_the_survival_and_inflammatory_potential_of_Candida_spp_involved_in_the_pathogenesis_of_chemotherapy_induced_oral_mucositis","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":32099627,"first_name":"Michele","middle_initials":"","last_name":"Tanturli","page_name":"MicheleTanturli","domain_name":"unifi","created_at":"2015-06-11T07:46:56.944-07:00","display_name":"Michele Tanturli","url":"https://unifi.academia.edu/MicheleTanturli"},"attachments":[],"research_interests":[{"id":23940,"name":"Near Infrared","url":"https://www.academia.edu/Documents/in/Near_Infrared"},{"id":105582,"name":"Candida","url":"https://www.academia.edu/Documents/in/Candida"},{"id":131573,"name":"Candida albicans","url":"https://www.academia.edu/Documents/in/Candida_albicans"},{"id":335966,"name":"Candida parapsilosis","url":"https://www.academia.edu/Documents/in/Candida_parapsilosis"},{"id":550226,"name":"Oral mucositis","url":"https://www.academia.edu/Documents/in/Oral_mucositis"},{"id":1607687,"name":"Chemotherapy-induced mucositis","url":"https://www.academia.edu/Documents/in/Chemotherapy-induced_mucositis"}],"urls":[{"id":5773729,"url":"http://www.ncbi.nlm.nih.gov/pubmed/26173694"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059713"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059713/Effects_of_soluble_extracts_from_Leishmania_infantum_promastigotes_Toxoplasma_gondii_tachyzoites_on_TGF_b_mediated_pathways_in_activated_CD4_%C3%BE_T_lymphocytes"><img alt="Research paper thumbnail of Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes" class="work-thumbnail" src="https://attachments.academia-assets.com/55945235/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059713/Effects_of_soluble_extracts_from_Leishmania_infantum_promastigotes_Toxoplasma_gondii_tachyzoites_on_TGF_b_mediated_pathways_in_activated_CD4_%C3%BE_T_lymphocytes">Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CSeverini1">C. Severini</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Interference with transforming growth factor-b-mediated pathways helps several parasites to survi...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="52a4ff6a09f010d0a9710ac38f9db08d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945235,"asset_id":36059713,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945235/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059713"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059713"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059713; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059713]").text(description); $(".js-view-count[data-work-id=36059713]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059713; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059713']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059713, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "52a4ff6a09f010d0a9710ac38f9db08d" } } $('.js-work-strip[data-work-id=36059713]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059713,"title":"Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes","translated_title":"","metadata":{"abstract":"Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells."},"translated_abstract":"Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells.","internal_url":"https://www.academia.edu/36059713/Effects_of_soluble_extracts_from_Leishmania_infantum_promastigotes_Toxoplasma_gondii_tachyzoites_on_TGF_b_mediated_pathways_in_activated_CD4_%C3%BE_T_lymphocytes","translated_internal_url":"","created_at":"2018-03-02T05:52:29.362-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136597,"work_id":36059713,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes"},{"id":31136598,"work_id":36059713,"tagging_user_id":32025990,"tagged_user_id":32099627,"co_author_invite_id":null,"email":"m***i@unifi.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":2,"name":"Michele Tanturli","title":"Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes"},{"id":31136599,"work_id":36059713,"tagging_user_id":32025990,"tagged_user_id":37775023,"co_author_invite_id":null,"email":"s***i@iss.it","display_order":3,"name":"C. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059757"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059757/Stimulatory_Interactions_between_Human_Coronary_Smooth_Muscle_Cells_and_Dendritic_Cells"><img alt="Research paper thumbnail of Stimulatory Interactions between Human Coronary Smooth Muscle Cells and Dendritic Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/55945286/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059757/Stimulatory_Interactions_between_Human_Coronary_Smooth_Muscle_Cells_and_Dendritic_Cells">Stimulatory Interactions between Human Coronary Smooth Muscle Cells and Dendritic Cells</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Despite inflammatory and immune mechanisms participating to atherogenesis and dendritic cells (DC...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Despite inflammatory and immune mechanisms participating to atherogenesis and dendritic cells (DCs) driving immune and non-immune tissue injury response, the interactions between DCs and vascular smooth muscle cells (VSMCs) possibly relevant to vascular pathology including atherogenesis are still unclear. To address this issue, immature DCs (iDCs) generated from CD14 + cells isolated from healthy donors were matured either with cytokines (mDCs), or co-cultured (ccDCs) with human coronary artery VSMCs (CASMCs) using transwell chambers. Co-culture induced DC immunophenotypical and functional maturation similar to cytokines, as demonstrated by flow cytometry and mixed lymphocyte reaction. In turn, factors from mDCs and ccDCs induced CASMC migration. MCP-1 and TNFa, secreted from DCs, and IL-6 and MCP-1, secreted from CASMCs, were primarily involved. mDCs adhesion to CASMCs was enhanced by CASMC pre-treatment with IFNc and TNFa ICAM-1 and VCAM-1 were involved, since the expression of specific mRNAs for these molecules increased and adhesion was inhibited by neutralizing antibodies to the counter-receptors CD11c and CD18. Adhesion was also inhibited by CASMC pre-treatment with the HMG-CoA-reductase inhibitor atorvastatin and the PPARc agonist rosiglitazone, which suggests a further mechanism for the anti-inflammatory action of these drugs. Adhesion of DCs to VSMCs was shown also in vivo in rat carotid 7 to 21 days after crush and incision injury. The findings indicate that DCs and VSMCs can interact with reciprocal stimulation, possibly leading to perpetuate inflammation and vascular wall remodelling, and that the interaction is enhanced by a cytokine-rich inflammatory environment and down-regulated by HMGCoA-reductase inhibitors and PPARc agonists.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bdec44db94d2c0bc39101cad162891e7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945286,"asset_id":36059757,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945286/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059757"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059757"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059757; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059757]").text(description); $(".js-view-count[data-work-id=36059757]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059757; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059757']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059757, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bdec44db94d2c0bc39101cad162891e7" } } $('.js-work-strip[data-work-id=36059757]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059757,"title":"Stimulatory Interactions between Human Coronary Smooth Muscle Cells and Dendritic Cells","translated_title":"","metadata":{"abstract":"Despite inflammatory and immune mechanisms participating to atherogenesis and dendritic cells (DCs) driving immune and non-immune tissue injury response, the interactions between DCs and vascular smooth muscle cells (VSMCs) possibly relevant to vascular pathology including atherogenesis are still unclear. To address this issue, immature DCs (iDCs) generated from CD14 + cells isolated from healthy donors were matured either with cytokines (mDCs), or co-cultured (ccDCs) with human coronary artery VSMCs (CASMCs) using transwell chambers. Co-culture induced DC immunophenotypical and functional maturation similar to cytokines, as demonstrated by flow cytometry and mixed lymphocyte reaction. In turn, factors from mDCs and ccDCs induced CASMC migration. MCP-1 and TNFa, secreted from DCs, and IL-6 and MCP-1, secreted from CASMCs, were primarily involved. mDCs adhesion to CASMCs was enhanced by CASMC pre-treatment with IFNc and TNFa ICAM-1 and VCAM-1 were involved, since the expression of specific mRNAs for these molecules increased and adhesion was inhibited by neutralizing antibodies to the counter-receptors CD11c and CD18. Adhesion was also inhibited by CASMC pre-treatment with the HMG-CoA-reductase inhibitor atorvastatin and the PPARc agonist rosiglitazone, which suggests a further mechanism for the anti-inflammatory action of these drugs. Adhesion of DCs to VSMCs was shown also in vivo in rat carotid 7 to 21 days after crush and incision injury. The findings indicate that DCs and VSMCs can interact with reciprocal stimulation, possibly leading to perpetuate inflammation and vascular wall remodelling, and that the interaction is enhanced by a cytokine-rich inflammatory environment and down-regulated by HMGCoA-reductase inhibitors and PPARc agonists."},"translated_abstract":"Despite inflammatory and immune mechanisms participating to atherogenesis and dendritic cells (DCs) driving immune and non-immune tissue injury response, the interactions between DCs and vascular smooth muscle cells (VSMCs) possibly relevant to vascular pathology including atherogenesis are still unclear. To address this issue, immature DCs (iDCs) generated from CD14 + cells isolated from healthy donors were matured either with cytokines (mDCs), or co-cultured (ccDCs) with human coronary artery VSMCs (CASMCs) using transwell chambers. Co-culture induced DC immunophenotypical and functional maturation similar to cytokines, as demonstrated by flow cytometry and mixed lymphocyte reaction. In turn, factors from mDCs and ccDCs induced CASMC migration. MCP-1 and TNFa, secreted from DCs, and IL-6 and MCP-1, secreted from CASMCs, were primarily involved. mDCs adhesion to CASMCs was enhanced by CASMC pre-treatment with IFNc and TNFa ICAM-1 and VCAM-1 were involved, since the expression of specific mRNAs for these molecules increased and adhesion was inhibited by neutralizing antibodies to the counter-receptors CD11c and CD18. Adhesion was also inhibited by CASMC pre-treatment with the HMG-CoA-reductase inhibitor atorvastatin and the PPARc agonist rosiglitazone, which suggests a further mechanism for the anti-inflammatory action of these drugs. Adhesion of DCs to VSMCs was shown also in vivo in rat carotid 7 to 21 days after crush and incision injury. The findings indicate that DCs and VSMCs can interact with reciprocal stimulation, possibly leading to perpetuate inflammation and vascular wall remodelling, and that the interaction is enhanced by a cytokine-rich inflammatory environment and down-regulated by HMGCoA-reductase inhibitors and PPARc agonists.","internal_url":"https://www.academia.edu/36059757/Stimulatory_Interactions_between_Human_Coronary_Smooth_Muscle_Cells_and_Dendritic_Cells","translated_internal_url":"","created_at":"2018-03-02T06:00:15.548-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136623,"work_id":36059757,"tagging_user_id":32025990,"tagged_user_id":17404428,"co_author_invite_id":null,"email":"s***0@yahoo.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":1,"name":"Sara Paccosi","title":"Stimulatory Interactions between Human Coronary 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059766"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059766/Modulation_of_the_Immune_and_Inflammatory_Responses_by_Plasmodium_falciparum_Schizont_Extracts_Role_of_Myeloid_Dendritic_Cells_in_Effector_and_Regulatory_Functions_of_CD4_Lymphocytes"><img alt="Research paper thumbnail of Modulation of the Immune and Inflammatory Responses by Plasmodium falciparum Schizont Extracts: Role of Myeloid Dendritic Cells in Effector and Regulatory Functions of CD4 Lymphocytes" class="work-thumbnail" src="https://attachments.academia-assets.com/55945299/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059766/Modulation_of_the_Immune_and_Inflammatory_Responses_by_Plasmodium_falciparum_Schizont_Extracts_Role_of_Myeloid_Dendritic_Cells_in_Effector_and_Regulatory_Functions_of_CD4_Lymphocytes">Modulation of the Immune and Inflammatory Responses by Plasmodium falciparum Schizont Extracts: Role of Myeloid Dendritic Cells in Effector and Regulatory Functions of CD4 Lymphocytes</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The optimal immune response to malaria infection comprises rapid induction of inflammatory respon...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The optimal immune response to malaria infection comprises rapid induction of inflammatory responses promptly counteracted by regulatory mechanisms to prevent immunopathology. To evaluate the role of dendritic cells (DC) in the balance of parasite induced inflammatory/anti-inflammatory mechanisms, we studied the activity of monocyte-derived dendritic cells (MDDC), previously exposed to soluble extracts of Plasmodium falciparum-infected red blood cells (PfSE), in the differentiation of CD4 cells isolated from donors never exposed to malaria infection. We show that MDDC exposed to PfSE are extremely efficient to induce a contemporary differentiation of TH1 effector cells and T regulatory (Treg) cells in CD4 T cells even when exposed to low concentrations of parasitic extracts. Treg cells induced by MDDC infected with PfSE (MDDC-PfSE) produce transforming growth factor beta (TGF-) and interleukin 10 (IL-10) and are endowed with strong suppressive properties. They also show phenotypical and functional peculiarities, such as the contemporary expression of markers of Treg and TH1 differentiation and higher sensitivity to TLR4 ligands both inducing an increasing production of suppressive cytokines. On the whole, our data indicate that MDDC exposed to PfSE orchestrate a well-balanced immune response with timely differentiation of TH1 and Treg cells in CD4 cells from nonimmune donors and suggest that, during the infection, the role of MDCC could be particularly relevant in low-parasitemia conditions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="83064e5959971113151f489763a1176d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945299,"asset_id":36059766,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945299/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059766"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059766"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059766; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059766]").text(description); $(".js-view-count[data-work-id=36059766]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059766; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059766']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059766, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "83064e5959971113151f489763a1176d" } } $('.js-work-strip[data-work-id=36059766]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059766,"title":"Modulation of the Immune and Inflammatory Responses by Plasmodium falciparum Schizont Extracts: Role of Myeloid Dendritic Cells in Effector and Regulatory Functions of CD4 Lymphocytes","translated_title":"","metadata":{"abstract":"The optimal immune response to malaria infection comprises rapid induction of inflammatory responses promptly counteracted by regulatory mechanisms to prevent immunopathology. To evaluate the role of dendritic cells (DC) in the balance of parasite induced inflammatory/anti-inflammatory mechanisms, we studied the activity of monocyte-derived dendritic cells (MDDC), previously exposed to soluble extracts of Plasmodium falciparum-infected red blood cells (PfSE), in the differentiation of CD4 cells isolated from donors never exposed to malaria infection. We show that MDDC exposed to PfSE are extremely efficient to induce a contemporary differentiation of TH1 effector cells and T regulatory (Treg) cells in CD4 T cells even when exposed to low concentrations of parasitic extracts. Treg cells induced by MDDC infected with PfSE (MDDC-PfSE) produce transforming growth factor beta (TGF-) and interleukin 10 (IL-10) and are endowed with strong suppressive properties. They also show phenotypical and functional peculiarities, such as the contemporary expression of markers of Treg and TH1 differentiation and higher sensitivity to TLR4 ligands both inducing an increasing production of suppressive cytokines. On the whole, our data indicate that MDDC exposed to PfSE orchestrate a well-balanced immune response with timely differentiation of TH1 and Treg cells in CD4 cells from nonimmune donors and suggest that, during the infection, the role of MDCC could be particularly relevant in low-parasitemia conditions."},"translated_abstract":"The optimal immune response to malaria infection comprises rapid induction of inflammatory responses promptly counteracted by regulatory mechanisms to prevent immunopathology. To evaluate the role of dendritic cells (DC) in the balance of parasite induced inflammatory/anti-inflammatory mechanisms, we studied the activity of monocyte-derived dendritic cells (MDDC), previously exposed to soluble extracts of Plasmodium falciparum-infected red blood cells (PfSE), in the differentiation of CD4 cells isolated from donors never exposed to malaria infection. We show that MDDC exposed to PfSE are extremely efficient to induce a contemporary differentiation of TH1 effector cells and T regulatory (Treg) cells in CD4 T cells even when exposed to low concentrations of parasitic extracts. Treg cells induced by MDDC infected with PfSE (MDDC-PfSE) produce transforming growth factor beta (TGF-) and interleukin 10 (IL-10) and are endowed with strong suppressive properties. 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059777"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059777/Haematological_parameters_natural_regulatory_CD4_CD25_FOXP3"><img alt="Research paper thumbnail of Haematological parameters natural regulatory CD4 CD25 FOXP3" class="work-thumbnail" src="https://attachments.academia-assets.com/55945312/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059777/Haematological_parameters_natural_regulatory_CD4_CD25_FOXP3">Haematological parameters natural regulatory CD4 CD25 FOXP3</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/MaritaTroyeblomberg">Marita Troye-blomberg</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Haematological parameters, natural regulatory CD4 + CD25 + FOXP3+ T cells and gδ T cells among tw...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Haematological parameters, natural regulatory CD4 + CD25 + FOXP3+ T cells and gδ T cells among two sympatric ethnic groups having different susceptibility to malaria in Burkina Faso Abstract Background: Fulani ethnic group individuals are less susceptible than sympatric Mossi ethnic group, in term of malaria infection severity, and differ in antibody production against malaria antigens. The differences in susceptibility to malaria between Fulani and Mossi ethnic groups are thought to be regulated by different genetic backgrounds and offer the opportunity to compare haematological parameters, Tregs and gδT cell profiles in seasonal and stable malaria transmission settings in Burkina Faso. The study was conducted at two different time points i.e. during the high and low malaria transmission period. Results: Two cross-sectional surveys were undertaken in adults above 20 years belonging either to the Fulani or the Mossi ethnic groups 1) at the peak of the malaria transmission season and 2) during the middle of the low malaria transmission season. Full blood counts, proportions of Tregs and gδ T cells were measured at both time-points. As previously shown the Fulani and Mossi ethnic groups showed a consistent difference in P. falciparum infection rates and parasite load. Differential white blood cell counts showed that the absolute lymphocyte counts were higher in the Mossi than in the Fulani ethnic group at both time points. While the proportion of CD4+CD25 high was higher in the Fulani ethnic group at the peak of malaria transmission season (p = 0.03), no clear pattern emerged for T regulatory cells expressing FoxP3 + and CD127 low. However CD3 + gδ + subpopulations were found to be higher in the Fulani compared to the Mossi ethnic group, and this difference was statistically significant at both time-points (p = 0.004 at low transmission season and p = 0.04 at peak of transmission). Conclusion: Our findings on regulatory T cell phenotypes suggest an interesting role for immune regulatory mechanisms in response to malaria. The study also suggests that TCRgδ + cells might contribute to the protection against malaria in the Fulani ethnic group involving their reported parasite inhibitory activities.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4c3bf9a215cf1cbbe3f50eb258000323" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945312,"asset_id":36059777,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945312/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059777"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059777"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059777; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059777]").text(description); $(".js-view-count[data-work-id=36059777]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059777; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059777']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059777, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "4c3bf9a215cf1cbbe3f50eb258000323" } } $('.js-work-strip[data-work-id=36059777]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059777,"title":"Haematological parameters natural regulatory CD4 CD25 FOXP3","translated_title":"","metadata":{"abstract":"Haematological parameters, natural regulatory CD4 + CD25 + FOXP3+ T cells and gδ T cells among two sympatric ethnic groups having different susceptibility to malaria in Burkina Faso Abstract Background: Fulani ethnic group individuals are less susceptible than sympatric Mossi ethnic group, in term of malaria infection severity, and differ in antibody production against malaria antigens. The differences in susceptibility to malaria between Fulani and Mossi ethnic groups are thought to be regulated by different genetic backgrounds and offer the opportunity to compare haematological parameters, Tregs and gδT cell profiles in seasonal and stable malaria transmission settings in Burkina Faso. The study was conducted at two different time points i.e. during the high and low malaria transmission period. Results: Two cross-sectional surveys were undertaken in adults above 20 years belonging either to the Fulani or the Mossi ethnic groups 1) at the peak of the malaria transmission season and 2) during the middle of the low malaria transmission season. Full blood counts, proportions of Tregs and gδ T cells were measured at both time-points. As previously shown the Fulani and Mossi ethnic groups showed a consistent difference in P. falciparum infection rates and parasite load. Differential white blood cell counts showed that the absolute lymphocyte counts were higher in the Mossi than in the Fulani ethnic group at both time points. While the proportion of CD4+CD25 high was higher in the Fulani ethnic group at the peak of malaria transmission season (p = 0.03), no clear pattern emerged for T regulatory cells expressing FoxP3 + and CD127 low. However CD3 + gδ + subpopulations were found to be higher in the Fulani compared to the Mossi ethnic group, and this difference was statistically significant at both time-points (p = 0.004 at low transmission season and p = 0.04 at peak of transmission). Conclusion: Our findings on regulatory T cell phenotypes suggest an interesting role for immune regulatory mechanisms in response to malaria. The study also suggests that TCRgδ + cells might contribute to the protection against malaria in the Fulani ethnic group involving their reported parasite inhibitory activities."},"translated_abstract":"Haematological parameters, natural regulatory CD4 + CD25 + FOXP3+ T cells and gδ T cells among two sympatric ethnic groups having different susceptibility to malaria in Burkina Faso Abstract Background: Fulani ethnic group individuals are less susceptible than sympatric Mossi ethnic group, in term of malaria infection severity, and differ in antibody production against malaria antigens. The differences in susceptibility to malaria between Fulani and Mossi ethnic groups are thought to be regulated by different genetic backgrounds and offer the opportunity to compare haematological parameters, Tregs and gδT cell profiles in seasonal and stable malaria transmission settings in Burkina Faso. The study was conducted at two different time points i.e. during the high and low malaria transmission period. Results: Two cross-sectional surveys were undertaken in adults above 20 years belonging either to the Fulani or the Mossi ethnic groups 1) at the peak of the malaria transmission season and 2) during the middle of the low malaria transmission season. Full blood counts, proportions of Tregs and gδ T cells were measured at both time-points. As previously shown the Fulani and Mossi ethnic groups showed a consistent difference in P. falciparum infection rates and parasite load. Differential white blood cell counts showed that the absolute lymphocyte counts were higher in the Mossi than in the Fulani ethnic group at both time points. While the proportion of CD4+CD25 high was higher in the Fulani ethnic group at the peak of malaria transmission season (p = 0.03), no clear pattern emerged for T regulatory cells expressing FoxP3 + and CD127 low. However CD3 + gδ + subpopulations were found to be higher in the Fulani compared to the Mossi ethnic group, and this difference was statistically significant at both time-points (p = 0.004 at low transmission season and p = 0.04 at peak of transmission). Conclusion: Our findings on regulatory T cell phenotypes suggest an interesting role for immune regulatory mechanisms in response to malaria. 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text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36090518/Interferon_a_and_Interleukin_2_Synergistically_Enhance_Basic_Fibroblast_Growth_Factor_Synthesis_and_Induce_Release_Promoting_Endothelial_Cell_Growth">Interferon-a and Interleukin 2 Synergistically Enhance Basic Fibroblast Growth Factor Synthesis and Induce Release, Promoting Endothelial Cell Growth</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To elucidate mechanisms underlying neovascularization that accompanies certain chronic immune/ in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To elucidate mechanisms underlying neovascularization that accompanies certain chronic immune/ inflammatory disorders, the effects of interferon-a (IFN-a) and interleukin 2 (IL-2) on endothelial cell (EC) growth in vitro and angiogenesis in vivo were studied. Preincubation of cultured human ECs with IFN-a, followed by exposure to IL-2, resulted in effective stimulation of cell growth, whereas either cytokine alone had only a slight effect. The combination of IFN-a/IL-2 induced an an-giogenic response in the rabbit cornea. IL-2 receptor expression was enhanced on IFN-a-treated ECs: p55 was increased and p70 was induced. '25I-IL-2 binding to ECs treated with IFN-a was enhanced (Kd from 7 nM to 260 pM with IFN-a), and anti-p55 IgG blocked '25I-IL-2/EC interaction as well as IL-2-mediated EC proliferation. Consistent with these findings in cell culture, immunohistologic studies demonstrated p55 and p70 antigen in the vasculature of rheumatoid joints, but not in normal joint tissue. Exposure of cultured ECs to IFN-a increased levels of intracellular EC basic fibroblast growth factor (bFGF), and subsequent addition of IL-2 led to bFGF release into the medium. The observation that anti-bFGF IgG largely blocked EC proliferation in response to IFN-a/IL-2 suggested that bFGF was a critical agent in this setting. These data suggest a mechanism rendering ECs responsive to IL-2 which may be relevant in immune/inflammatory disorders: IFN-a-mediated induction of functional EC receptors for IL-2, which drives cell proliferation by a mechanism dependent on increased synthesis and release of bFGF. (J. Clin. Invest. 1993. 91:2504-2512.)</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f0e6c1a7dfbbc49d1906727956ee4a78" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55980090,"asset_id":36090518,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55980090/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36090518"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36090518"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36090518; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36090518]").text(description); $(".js-view-count[data-work-id=36090518]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36090518; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36090518']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36090518, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "f0e6c1a7dfbbc49d1906727956ee4a78" } } $('.js-work-strip[data-work-id=36090518]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36090518,"title":"Interferon-a and Interleukin 2 Synergistically Enhance Basic Fibroblast Growth Factor Synthesis and Induce Release, Promoting Endothelial Cell Growth","translated_title":"","metadata":{"abstract":"To elucidate mechanisms underlying neovascularization that accompanies certain chronic immune/ inflammatory disorders, the effects of interferon-a (IFN-a) and interleukin 2 (IL-2) on endothelial cell (EC) growth in vitro and angiogenesis in vivo were studied. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059786"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059786/Sex_Differences_in_the_Response_to_Viral_Infections_TLR8_and_TLR9_Ligand_Stimulation_Induce_Higher_IL10_Production_in_Males"><img alt="Research paper thumbnail of Sex Differences in the Response to Viral Infections: TLR8 and TLR9 Ligand Stimulation Induce Higher IL10 Production in Males" class="work-thumbnail" src="https://attachments.academia-assets.com/55945323/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059786/Sex_Differences_in_the_Response_to_Viral_Infections_TLR8_and_TLR9_Ligand_Stimulation_Induce_Higher_IL10_Production_in_Males">Sex Differences in the Response to Viral Infections: TLR8 and TLR9 Ligand Stimulation Induce Higher IL10 Production in Males</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/LiviaCivitelli">Livia Civitelli</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background: Susceptibility to viral infections as well as their severity are higher in men than i...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background: Susceptibility to viral infections as well as their severity are higher in men than in women. Heightened antiviral responses typical of women are effective for rapid virus clearance, but if excessively high or prolonged, can result in chronic/ inflammatory pathologies. We investigated whether this variability could be in part attributable to differences in the response to the Toll-Like Receptors (TLR) more involved in the virus recognition.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="93a164ac713ea36782f898793c0d5f39" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945323,"asset_id":36059786,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945323/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059786"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059786"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059786; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059786]").text(description); $(".js-view-count[data-work-id=36059786]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059786; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059786']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059786, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "93a164ac713ea36782f898793c0d5f39" } } $('.js-work-strip[data-work-id=36059786]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059786,"title":"Sex Differences in the Response to Viral Infections: TLR8 and TLR9 Ligand Stimulation Induce Higher IL10 Production in Males","translated_title":"","metadata":{"abstract":"Background: Susceptibility to viral infections as well as their severity are higher in men than in women. 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wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059803/Low_molecular_weight_non_peptidic_agonists_of_TrkA_receptor_with_NGF_mimetic_activity">Low molecular weight, non-peptidic agonists of TrkA receptor with NGF-mimetic activity</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Exploitation of the biologic activity of neurotrophins is desirable for medical purposes, but the...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Exploitation of the biologic activity of neurotrophins is desirable for medical purposes, but their protein nature intrinsically bears adverse pharmacokinetic properties. Here, we report synthesis and biologic characterization of a novel class of low molecular weight, non-peptidic compounds with NGF (nerve growth factor)-mimetic properties. MT2, a representative compound, bound to Trk (tropomyosin kinase receptor)A chain on NGF-sensitive cells, as well as in cell-free assays, at nanomolar concentrations and induced TrkA autophosphorylation and receptor-mediated internalization. MT2 binding involved at least two amino-acid residues within TrkA molecule. Like NGF, MT2 increased phosphorylation of extracellular signal-regulated kinase1/2 and Akt proteins and production of MKP-1 phosphatase (dual specificity phosphatase 1), modulated p38 mitogen-activated protein kinase activation, sustained survival of serum-starved PC12 or RDG cells, and promoted their differentiation. However, the intensity of such responses was heterogenous, as the ability of maintaining survival was equally possessed by NGF and MT2, whereas the induction of differentiation was expressed at definitely lower levels by the mimetic. Analysis of TrkA autophosphorylation patterns induced by MT2 revealed a strong tyrosine (Tyr)490 and a limited Tyr785 and Tyr674/675 activation, findings coherent with the observed functional divarication. Consistently, in an NGF-deprived rat hippocampal neuronal model of Alzheimer Disease, MT2 could correct the biochemical abnormalities and sustain cell survival. Thus, NGF mimetics may reveal interesting investigational tools in neurobiology, as well as promising drug candidates.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0a9b634c9553da9cdeb12c5e129ddedb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945341,"asset_id":36059803,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945341/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059803"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059803"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059803; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059803]").text(description); $(".js-view-count[data-work-id=36059803]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059803; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059803']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059803, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0a9b634c9553da9cdeb12c5e129ddedb" } } $('.js-work-strip[data-work-id=36059803]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059803,"title":"Low molecular weight, non-peptidic agonists of TrkA receptor with NGF-mimetic activity","translated_title":"","metadata":{"abstract":"Exploitation of the biologic activity of neurotrophins is desirable for medical purposes, but their protein nature intrinsically bears adverse pharmacokinetic properties. Here, we report synthesis and biologic characterization of a novel class of low molecular weight, non-peptidic compounds with NGF (nerve growth factor)-mimetic properties. MT2, a representative compound, bound to Trk (tropomyosin kinase receptor)A chain on NGF-sensitive cells, as well as in cell-free assays, at nanomolar concentrations and induced TrkA autophosphorylation and receptor-mediated internalization. MT2 binding involved at least two amino-acid residues within TrkA molecule. Like NGF, MT2 increased phosphorylation of extracellular signal-regulated kinase1/2 and Akt proteins and production of MKP-1 phosphatase (dual specificity phosphatase 1), modulated p38 mitogen-activated protein kinase activation, sustained survival of serum-starved PC12 or RDG cells, and promoted their differentiation. 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However, the intensity of such responses was heterogenous, as the ability of maintaining survival was equally possessed by NGF and MT2, whereas the induction of differentiation was expressed at definitely lower levels by the mimetic. Analysis of TrkA autophosphorylation patterns induced by MT2 revealed a strong tyrosine (Tyr)490 and a limited Tyr785 and Tyr674/675 activation, findings coherent with the observed functional divarication. Consistently, in an NGF-deprived rat hippocampal neuronal model of Alzheimer Disease, MT2 could correct the biochemical abnormalities and sustain cell survival. 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class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059824/Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive_function_of_polyclonal_T_regulatory_cells_through_activation_of_TGFb_mediated_signals">Plasmodium falciparum soluble extracts potentiate the suppressive function of polyclonal T regulatory cells through activation of TGFb-mediated signals</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AnnmariaClemente">Annmaria Clemente</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Increased numbers of T regulatory cells (Tregs), key mediators of immune homeostasis, were report...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Increased numbers of T regulatory cells (Tregs), key mediators of immune homeostasis, were reported in human and murine malaria and it is current opinion that these cells play a role in balancing protective immunity and pathogenesis during infection. However, the mechanisms governing their expansion during malaria infection are not completely defined. In this article we show that soluble extracts of Plasmodium falciparum (PfSEs), but not equivalent preparation of uninfected eryth-rocytes, induce the differentiation of polyclonally activated CD4 + cells in Tregs endowed with strong suppressive activity. PfSEs activate latent TGFb bound on the membrane of Treg cells, thus allowing the cytokine interaction with TGFb receptor, and inducing Foxp3 gene expression and TGFb production. The activation of membrane-bound latent TGFb by PfSEs is significantly reduced by a broad-spectrum metalloproteinases inhibitor with Zn ++-chelating activity, and completely inhibited by the combined action of such inhibitor and antibodies to a P. falciparum thrombospondin-related adhesive protein (PfTRAP). We conclude that Pf-Zn ++-dependent proteinases and, to a lesser extent, PfTRAP molecules are involved in the activation of latent TGFb bound on the membrane of activated Treg cells and suggest that, in malaria infection, this mechanism could contribute to the expansion of Tregs with different antigen specificity.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="81a150507b60446d9360e49702abfa4c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945361,"asset_id":36059824,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945361/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059824"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059824"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059824; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059824]").text(description); $(".js-view-count[data-work-id=36059824]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059824; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059824']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059824, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "81a150507b60446d9360e49702abfa4c" } } $('.js-work-strip[data-work-id=36059824]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059824,"title":"Plasmodium falciparum soluble extracts potentiate the suppressive function of polyclonal T regulatory cells through activation of TGFb-mediated signals","translated_title":"","metadata":{"abstract":"Increased numbers of T regulatory cells (Tregs), key mediators of immune homeostasis, were reported in human and murine malaria and it is current opinion that these cells play a role in balancing protective immunity and pathogenesis during infection. However, the mechanisms governing their expansion during malaria infection are not completely defined. In this article we show that soluble extracts of Plasmodium falciparum (PfSEs), but not equivalent preparation of uninfected eryth-rocytes, induce the differentiation of polyclonally activated CD4 + cells in Tregs endowed with strong suppressive activity. PfSEs activate latent TGFb bound on the membrane of Treg cells, thus allowing the cytokine interaction with TGFb receptor, and inducing Foxp3 gene expression and TGFb production. The activation of membrane-bound latent TGFb by PfSEs is significantly reduced by a broad-spectrum metalloproteinases inhibitor with Zn ++-chelating activity, and completely inhibited by the combined action of such inhibitor and antibodies to a P. falciparum thrombospondin-related adhesive protein (PfTRAP). We conclude that Pf-Zn ++-dependent proteinases and, to a lesser extent, PfTRAP molecules are involved in the activation of latent TGFb bound on the membrane of activated Treg cells and suggest that, in malaria infection, this mechanism could contribute to the expansion of Tregs with different antigen specificity."},"translated_abstract":"Increased numbers of T regulatory cells (Tregs), key mediators of immune homeostasis, were reported in human and murine malaria and it is current opinion that these cells play a role in balancing protective immunity and pathogenesis during infection. However, the mechanisms governing their expansion during malaria infection are not completely defined. In this article we show that soluble extracts of Plasmodium falciparum (PfSEs), but not equivalent preparation of uninfected eryth-rocytes, induce the differentiation of polyclonally activated CD4 + cells in Tregs endowed with strong suppressive activity. PfSEs activate latent TGFb bound on the membrane of Treg cells, thus allowing the cytokine interaction with TGFb receptor, and inducing Foxp3 gene expression and TGFb production. The activation of membrane-bound latent TGFb by PfSEs is significantly reduced by a broad-spectrum metalloproteinases inhibitor with Zn ++-chelating activity, and completely inhibited by the combined action of such inhibitor and antibodies to a P. falciparum thrombospondin-related adhesive protein (PfTRAP). We conclude that Pf-Zn ++-dependent proteinases and, to a lesser extent, PfTRAP molecules are involved in the activation of latent TGFb bound on the membrane of activated Treg cells and suggest that, in malaria infection, this mechanism could contribute to the expansion of Tregs with different antigen specificity.","internal_url":"https://www.academia.edu/36059824/Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive_function_of_polyclonal_T_regulatory_cells_through_activation_of_TGFb_mediated_signals","translated_internal_url":"","created_at":"2018-03-02T06:09:29.681-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136695,"work_id":36059824,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Plasmodium falciparum soluble extracts potentiate the suppressive function of polyclonal T regulatory cells through activation of TGFb-mediated signals"},{"id":31136696,"work_id":36059824,"tagging_user_id":32025990,"tagged_user_id":32097049,"co_author_invite_id":null,"email":"a***e@virgilio.it","display_order":2,"name":"Annmaria Clemente","title":"Plasmodium falciparum soluble extracts potentiate the suppressive function of polyclonal T regulatory cells through activation of TGFb-mediated signals"}],"downloadable_attachments":[{"id":55945361,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945361/thumbnails/1.jpg","file_name":"Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive.pdf","download_url":"https://www.academia.edu/attachments/55945361/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Plasmodium_falciparum_soluble_extracts_p.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945361/Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive-libre.pdf?1519999979=\u0026response-content-disposition=attachment%3B+filename%3DPlasmodium_falciparum_soluble_extracts_p.pdf\u0026Expires=1732404749\u0026Signature=etySaAlh7XU4FUF6aIz87wLF7bPWyXffrGsRrc4duBcJyALP6jR8oCACpyzUSmUWC6sSGKvH51Xvk0XVYYA8yFhBWkzDY17xSorKoX1QUveFZiR9aXcwgpQ7SO6yoWTGyOXYy24nEEV~qTHxNhrjCKU3bu6UQHhNFN6Xvi56OoxIXTrSMFIKE-Hse~hdCQAWWPMUqKEFp3psTJ-BBGYGhhIMllwenNmQWmZYfCZaZVNJHr0BbmTi66k-u~6v55ZmQGdSntjYRfB7Yrjc~CTNfj9a52I44uVy-w3N6cj5IRf5W2ipz79ltTO1Si3Kdu3-Pb0ltdtnzpzKZBMBH46qVg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive_function_of_polyclonal_T_regulatory_cells_through_activation_of_TGFb_mediated_signals","translated_slug":"","page_count":11,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945361,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945361/thumbnails/1.jpg","file_name":"Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive.pdf","download_url":"https://www.academia.edu/attachments/55945361/download_file?st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Plasmodium_falciparum_soluble_extracts_p.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945361/Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive-libre.pdf?1519999979=\u0026response-content-disposition=attachment%3B+filename%3DPlasmodium_falciparum_soluble_extracts_p.pdf\u0026Expires=1732404749\u0026Signature=etySaAlh7XU4FUF6aIz87wLF7bPWyXffrGsRrc4duBcJyALP6jR8oCACpyzUSmUWC6sSGKvH51Xvk0XVYYA8yFhBWkzDY17xSorKoX1QUveFZiR9aXcwgpQ7SO6yoWTGyOXYy24nEEV~qTHxNhrjCKU3bu6UQHhNFN6Xvi56OoxIXTrSMFIKE-Hse~hdCQAWWPMUqKEFp3psTJ-BBGYGhhIMllwenNmQWmZYfCZaZVNJHr0BbmTi66k-u~6v55ZmQGdSntjYRfB7Yrjc~CTNfj9a52I44uVy-w3N6cj5IRf5W2ipz79ltTO1Si3Kdu3-Pb0ltdtnzpzKZBMBH46qVg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7823,"name":"Malaria","url":"https://www.academia.edu/Documents/in/Malaria"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060162"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060162/Hypoxia_mediated_induction_of_acidic_basic_fibroblast_growth_factor_and_platelet_derived_growth_factor_in_mononuclear_phagocytes_stimulates_growth_of_hypoxic_endothelial_cells_endothelium_angiogenesis"><img alt="Research paper thumbnail of Hypoxia-mediated induction of acidic/basic fibroblast growth factor and platelet-derived growth factor in mononuclear phagocytes stimulates growth of hypoxic endothelial cells (endothelium/angiogenesis" class="work-thumbnail" src="https://attachments.academia-assets.com/55945762/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060162/Hypoxia_mediated_induction_of_acidic_basic_fibroblast_growth_factor_and_platelet_derived_growth_factor_in_mononuclear_phagocytes_stimulates_growth_of_hypoxic_endothelial_cells_endothelium_angiogenesis">Hypoxia-mediated induction of acidic/basic fibroblast growth factor and platelet-derived growth factor in mononuclear phagocytes stimulates growth of hypoxic endothelial cells (endothelium/angiogenesis</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Wound repair and tumor vascularization depend upon blood vessel growth into hypoxic tissue. Altho...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Wound repair and tumor vascularization depend upon blood vessel growth into hypoxic tissue. Although hypoxia slows endothelial cell (EC) proliferation and suppresses EC basic fibroblast growth factor (bFGF) expression , we report that macrophages (MPs) exposed to Po2 12-14 torr (1 torr = 1333 Pa) synthesize and release in a time-dependent manner platelet-derived growth factor (PDGF) and acidic/basic FGFs (a/bFGFs), which stimulate the growth of hypoxic ECs. Chromatography of hypoxic MP-conditioned medium on immobilized heparin with an ascending NaCl gradient resolved three peaks of mitogenic activity: activity of the first peak was neutralized by antibody to PDGF; activity of the second peak was neutralized by antibody to aFGF; and activity of the third peak was neutralized by antibody to bFGF. Metabolically labeled lysates and supernatants from MPs exposed to hypoxia showed increased synthesis and release of immunoprecipitable PDGF and a/bFGF in the absence of changes in cell viability. Possible involvement of a heme-containing oxygen sensor in MP elaboration of growth factors was suggested by the induction of bFGF and PDGF by normoxic MPs exposed to nickel or cobalt, although metabolic inhibitors such as sodium azide were without effect. These results suggest a paracrine model in which hypoxia stimulates MP release of PDGF and a/bFGF, inducing EC proliferation and potentially promoting angiogenesis in hypoxic environments.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8e7f7882c66714f0cde9ff6136db144c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945762,"asset_id":36060162,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945762/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060162"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060162"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060162; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060162]").text(description); $(".js-view-count[data-work-id=36060162]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060162; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060162']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060162, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "8e7f7882c66714f0cde9ff6136db144c" } } $('.js-work-strip[data-work-id=36060162]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060162,"title":"Hypoxia-mediated induction of acidic/basic fibroblast growth factor and platelet-derived growth factor in mononuclear phagocytes stimulates growth of hypoxic endothelial cells (endothelium/angiogenesis","translated_title":"","metadata":{"abstract":"Wound repair and tumor vascularization depend upon blood vessel growth into hypoxic tissue. Although hypoxia slows endothelial cell (EC) proliferation and suppresses EC basic fibroblast growth factor (bFGF) expression , we report that macrophages (MPs) exposed to Po2 12-14 torr (1 torr = 1333 Pa) synthesize and release in a time-dependent manner platelet-derived growth factor (PDGF) and acidic/basic FGFs (a/bFGFs), which stimulate the growth of hypoxic ECs. Chromatography of hypoxic MP-conditioned medium on immobilized heparin with an ascending NaCl gradient resolved three peaks of mitogenic activity: activity of the first peak was neutralized by antibody to PDGF; activity of the second peak was neutralized by antibody to aFGF; and activity of the third peak was neutralized by antibody to bFGF. Metabolically labeled lysates and supernatants from MPs exposed to hypoxia showed increased synthesis and release of immunoprecipitable PDGF and a/bFGF in the absence of changes in cell viability. Possible involvement of a heme-containing oxygen sensor in MP elaboration of growth factors was suggested by the induction of bFGF and PDGF by normoxic MPs exposed to nickel or cobalt, although metabolic inhibitors such as sodium azide were without effect. These results suggest a paracrine model in which hypoxia stimulates MP release of PDGF and a/bFGF, inducing EC proliferation and potentially promoting angiogenesis in hypoxic environments."},"translated_abstract":"Wound repair and tumor vascularization depend upon blood vessel growth into hypoxic tissue. Although hypoxia slows endothelial cell (EC) proliferation and suppresses EC basic fibroblast growth factor (bFGF) expression , we report that macrophages (MPs) exposed to Po2 12-14 torr (1 torr = 1333 Pa) synthesize and release in a time-dependent manner platelet-derived growth factor (PDGF) and acidic/basic FGFs (a/bFGFs), which stimulate the growth of hypoxic ECs. Chromatography of hypoxic MP-conditioned medium on immobilized heparin with an ascending NaCl gradient resolved three peaks of mitogenic activity: activity of the first peak was neutralized by antibody to PDGF; activity of the second peak was neutralized by antibody to aFGF; and activity of the third peak was neutralized by antibody to bFGF. Metabolically labeled lysates and supernatants from MPs exposed to hypoxia showed increased synthesis and release of immunoprecipitable PDGF and a/bFGF in the absence of changes in cell viability. Possible involvement of a heme-containing oxygen sensor in MP elaboration of growth factors was suggested by the induction of bFGF and PDGF by normoxic MPs exposed to nickel or cobalt, although metabolic inhibitors such as sodium azide were without effect. 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060143"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060143/Interferon_Induced_Inhibition_of_B16_Melanoma_Cell_Proliferation_Interference_with_the_bFGF_Autocrine_Growth_Circuit"><img alt="Research paper thumbnail of Interferon--Induced Inhibition of B16 Melanoma Cell Proliferation: Interference with the bFGF Autocrine Growth Circuit" class="work-thumbnail" src="https://attachments.academia-assets.com/55945737/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060143/Interferon_Induced_Inhibition_of_B16_Melanoma_Cell_Proliferation_Interference_with_the_bFGF_Autocrine_Growth_Circuit">Interferon--Induced Inhibition of B16 Melanoma Cell Proliferation: Interference with the bFGF Autocrine Growth Circuit</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The molecular mechanisms underlying the growth inhibition induced by interferon-(IFN-) in B16 mu-...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The molecular mechanisms underlying the growth inhibition induced by interferon-(IFN-) in B16 mu-rine melanoma cells were investigated. IFN-did not induce cell apoptosis, but strongly interfered with the synthesis of basic fibroblast growth factor (bFGF), which acts as an autocrine growth factor in this system. Inhibition of bFGF synthesis was observed at the same concentrations (50 –500 pM, 10 –100 U/ml) of IFN-able to induce growth arrest of B16 melanoma cells. Although the synthesis of acidic (a)FGF was only slightly affected by IFN-, the cytokine induced release of an aFGF-related low-molecular-weight pep-tide, which was able to interfere with bFGF binding to surface receptors. Thus, the molecular mechanisms of IFN-activity on melanoma cells include a specific modulation of the bFGF autocrine circuit.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bb88f68292eed20e8a501a632535d2dd" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945737,"asset_id":36060143,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945737/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060143"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060143"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060143; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060143]").text(description); $(".js-view-count[data-work-id=36060143]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060143; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060143']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060143, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bb88f68292eed20e8a501a632535d2dd" } } $('.js-work-strip[data-work-id=36060143]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060143,"title":"Interferon--Induced Inhibition of B16 Melanoma Cell Proliferation: Interference with the bFGF Autocrine Growth Circuit","translated_title":"","metadata":{"abstract":"The molecular mechanisms underlying the growth inhibition induced by interferon-(IFN-) in B16 mu-rine melanoma cells were investigated. IFN-did not induce cell apoptosis, but strongly interfered with the synthesis of basic fibroblast growth factor (bFGF), which acts as an autocrine growth factor in this system. Inhibition of bFGF synthesis was observed at the same concentrations (50 –500 pM, 10 –100 U/ml) of IFN-able to induce growth arrest of B16 melanoma cells. Although the synthesis of acidic (a)FGF was only slightly affected by IFN-, the cytokine induced release of an aFGF-related low-molecular-weight pep-tide, which was able to interfere with bFGF binding to surface receptors. Thus, the molecular mechanisms of IFN-activity on melanoma cells include a specific modulation of the bFGF autocrine circuit."},"translated_abstract":"The molecular mechanisms underlying the growth inhibition induced by interferon-(IFN-) in B16 mu-rine melanoma cells were investigated. IFN-did not induce cell apoptosis, but strongly interfered with the synthesis of basic fibroblast growth factor (bFGF), which acts as an autocrine growth factor in this system. Inhibition of bFGF synthesis was observed at the same concentrations (50 –500 pM, 10 –100 U/ml) of IFN-able to induce growth arrest of B16 melanoma cells. Although the synthesis of acidic (a)FGF was only slightly affected by IFN-, the cytokine induced release of an aFGF-related low-molecular-weight pep-tide, which was able to interfere with bFGF binding to surface receptors. Thus, the molecular mechanisms of IFN-activity on melanoma cells include a specific modulation of the bFGF autocrine circuit.","internal_url":"https://www.academia.edu/36060143/Interferon_Induced_Inhibition_of_B16_Melanoma_Cell_Proliferation_Interference_with_the_bFGF_Autocrine_Growth_Circuit","translated_internal_url":"","created_at":"2018-03-02T06:51:39.672-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136998,"work_id":36060143,"tagging_user_id":32025990,"tagged_user_id":35756305,"co_author_invite_id":null,"email":"l***i@uniroma1.it","affiliation":"Università degli Studi \"La Sapienza\" di Roma","display_order":1,"name":"Lucia Nencioni","title":"Interferon--Induced Inhibition of B16 Melanoma Cell Proliferation: Interference with the bFGF Autocrine Growth Circuit"},{"id":31136999,"work_id":36060143,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":2,"name":"Federico Cozzolino","title":"Interferon--Induced Inhibition of B16 Melanoma Cell Proliferation: Interference with the bFGF Autocrine Growth Circuit"}],"downloadable_attachments":[{"id":55945737,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945737/thumbnails/1.jpg","file_name":"Interferon-alpha-induced_inhibition_of_B16_melanoma_cell_proliferation.pdf","download_url":"https://www.academia.edu/attachments/55945737/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Interferon_Induced_Inhibition_of_B16_Mel.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945737/Interferon-alpha-induced_inhibition_of_B16_melanoma_cell_proliferation-libre.pdf?1520002623=\u0026response-content-disposition=attachment%3B+filename%3DInterferon_Induced_Inhibition_of_B16_Mel.pdf\u0026Expires=1732404750\u0026Signature=Lf8dmgTdfBAifLi6Aukj~fpMK8VBl~WjmAqgfO1kzMq~FjyBQPPjZyMylY8TBpM3HJlo3bcGzVHdtCa84guti4LcNMEEOxNxX30NhPz3cOM0v0SIgk765HxRoagKfKngrszKWzb~GNr4YK8f4Ics-t8RhE4eE7gSY9mb1Sl0i9vqlc8AsEy9CyuTMrYjeTDgVvB425zsXTm1yFpayL6HNjUmccylYmZAg~gp-kh3hojLOHJW3xsgEblHrLF-F2WDX40Trk4vIeRGHxlaeE0aCFktDhXhGjMU828AXJTIzquMdSMHH-XNXfHjxHauDXHX~dXWSCJffzKPEJB9W7zeGw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Interferon_Induced_Inhibition_of_B16_Melanoma_Cell_Proliferation_Interference_with_the_bFGF_Autocrine_Growth_Circuit","translated_slug":"","page_count":7,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945737,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945737/thumbnails/1.jpg","file_name":"Interferon-alpha-induced_inhibition_of_B16_melanoma_cell_proliferation.pdf","download_url":"https://www.academia.edu/attachments/55945737/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Interferon_Induced_Inhibition_of_B16_Mel.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945737/Interferon-alpha-induced_inhibition_of_B16_melanoma_cell_proliferation-libre.pdf?1520002623=\u0026response-content-disposition=attachment%3B+filename%3DInterferon_Induced_Inhibition_of_B16_Mel.pdf\u0026Expires=1732404750\u0026Signature=Lf8dmgTdfBAifLi6Aukj~fpMK8VBl~WjmAqgfO1kzMq~FjyBQPPjZyMylY8TBpM3HJlo3bcGzVHdtCa84guti4LcNMEEOxNxX30NhPz3cOM0v0SIgk765HxRoagKfKngrszKWzb~GNr4YK8f4Ics-t8RhE4eE7gSY9mb1Sl0i9vqlc8AsEy9CyuTMrYjeTDgVvB425zsXTm1yFpayL6HNjUmccylYmZAg~gp-kh3hojLOHJW3xsgEblHrLF-F2WDX40Trk4vIeRGHxlaeE0aCFktDhXhGjMU828AXJTIzquMdSMHH-XNXfHjxHauDXHX~dXWSCJffzKPEJB9W7zeGw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":188788,"name":"bFGF","url":"https://www.academia.edu/Documents/in/bFGF"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060130"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060130/NGF_Withdrawal_Induces_Apoptosis_in_CESS_B_Cell_Line_through_p38_MAPK_Activation_and_Bcl_2_Phosphorylation"><img alt="Research paper thumbnail of NGF Withdrawal Induces Apoptosis in CESS B Cell Line through p38 MAPK Activation and Bcl-2 Phosphorylation" class="work-thumbnail" src="https://attachments.academia-assets.com/55945726/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060130/NGF_Withdrawal_Induces_Apoptosis_in_CESS_B_Cell_Line_through_p38_MAPK_Activation_and_Bcl_2_Phosphorylation">NGF Withdrawal Induces Apoptosis in CESS B Cell Line through p38 MAPK Activation and Bcl-2 Phosphorylation</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/MariaLucibello">Maria Lucibello</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The sIgG lymphoblastoid B cell line CESS spontaneously produces a high amount of NGF and expresse...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The sIgG lymphoblastoid B cell line CESS spontaneously produces a high amount of NGF and expresses both high affinity (p140 Trk-A) and low affinity (p75 NTR) NGF receptors. Blocking NGF signals with neutralizing antibodies or specific Trk-A inhibitors induces a rapid phosphorylation of antiapoptotic Bcl-2 protein, followed by caspase activation, and apoptotic death of CESS cells. Bcl-2 phosphorylation in several sites within a 60 aa " loop " domain of protein is known to regulate its antiapoptotic function. Accordingly, CESS cells expressing the loop deletional mutant cDNA constructs Bcl-2 40-91 were completely resistant to apop-tosis induced by NGF withdrawal, indicating that Bcl-2 phosphorylation is a critical event. NGF withdrawal induces p38 MAPK, but not JNK, activation in CESS cells, and SB203580, a specific inhibitor of p38 MAPK, is able to prevent both Bcl-2 phosphorylation and apoptosis, indicating that p38 MAPK is the enzyme responsible for these events.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ccd884fbe68aa70742539bc9207e9723" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945726,"asset_id":36060130,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945726/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060130"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060130"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060130; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060130]").text(description); $(".js-view-count[data-work-id=36060130]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060130; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060130']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060130, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "ccd884fbe68aa70742539bc9207e9723" } } $('.js-work-strip[data-work-id=36060130]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060130,"title":"NGF Withdrawal Induces Apoptosis in CESS B Cell Line through p38 MAPK Activation and Bcl-2 Phosphorylation","translated_title":"","metadata":{"abstract":"The sIgG lymphoblastoid B cell line CESS spontaneously produces a high amount of NGF and expresses both high affinity (p140 Trk-A) and low affinity (p75 NTR) NGF receptors. Blocking NGF signals with neutralizing antibodies or specific Trk-A inhibitors induces a rapid phosphorylation of antiapoptotic Bcl-2 protein, followed by caspase activation, and apoptotic death of CESS cells. Bcl-2 phosphorylation in several sites within a 60 aa \" loop \" domain of protein is known to regulate its antiapoptotic function. Accordingly, CESS cells expressing the loop deletional mutant cDNA constructs Bcl-2 40-91 were completely resistant to apop-tosis induced by NGF withdrawal, indicating that Bcl-2 phosphorylation is a critical event. NGF withdrawal induces p38 MAPK, but not JNK, activation in CESS cells, and SB203580, a specific inhibitor of p38 MAPK, is able to prevent both Bcl-2 phosphorylation and apoptosis, indicating that p38 MAPK is the enzyme responsible for these events."},"translated_abstract":"The sIgG lymphoblastoid B cell line CESS spontaneously produces a high amount of NGF and expresses both high affinity (p140 Trk-A) and low affinity (p75 NTR) NGF receptors. Blocking NGF signals with neutralizing antibodies or specific Trk-A inhibitors induces a rapid phosphorylation of antiapoptotic Bcl-2 protein, followed by caspase activation, and apoptotic death of CESS cells. Bcl-2 phosphorylation in several sites within a 60 aa \" loop \" domain of protein is known to regulate its antiapoptotic function. Accordingly, CESS cells expressing the loop deletional mutant cDNA constructs Bcl-2 40-91 were completely resistant to apop-tosis induced by NGF withdrawal, indicating that Bcl-2 phosphorylation is a critical event. NGF withdrawal induces p38 MAPK, but not JNK, activation in CESS cells, and SB203580, a specific inhibitor of p38 MAPK, is able to prevent both Bcl-2 phosphorylation and apoptosis, indicating that p38 MAPK is the enzyme responsible for these events.","internal_url":"https://www.academia.edu/36060130/NGF_Withdrawal_Induces_Apoptosis_in_CESS_B_Cell_Line_through_p38_MAPK_Activation_and_Bcl_2_Phosphorylation","translated_internal_url":"","created_at":"2018-03-02T06:49:06.302-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136981,"work_id":36060130,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"NGF Withdrawal Induces Apoptosis in CESS B Cell Line through p38 MAPK Activation and Bcl-2 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060116"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060116/Nerve_Growth_Factor_Inhibits_Apoptosis_in_Memory_B_Lymphocytes_via_Inactivation_of_p38_MAPK_Prevention_of_Bcl_2_Phosphorylation_and_Cytochrome_c_Release"><img alt="Research paper thumbnail of Nerve Growth Factor Inhibits Apoptosis in Memory B Lymphocytes via Inactivation of p38 MAPK, Prevention of Bcl-2 Phosphorylation, and Cytochrome c Release" class="work-thumbnail" src="https://attachments.academia-assets.com/55945704/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060116/Nerve_Growth_Factor_Inhibits_Apoptosis_in_Memory_B_Lymphocytes_via_Inactivation_of_p38_MAPK_Prevention_of_Bcl_2_Phosphorylation_and_Cytochrome_c_Release">Nerve Growth Factor Inhibits Apoptosis in Memory B Lymphocytes via Inactivation of p38 MAPK, Prevention of Bcl-2 Phosphorylation, and Cytochrome c Release</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/SerenaAmmendola">Serena Ammendola</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Survival of memory B lymphocytes is tightly linked to the integrity of the Bcl-2 protein and is r...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Survival of memory B lymphocytes is tightly linked to the integrity of the Bcl-2 protein and is regulated by a nerve growth factor (NGF) autocrine circuit. In factor-starved memory B cells, the addition of exogenous NGF promptly induced p38 mitogen-activated protein kinase (MAPK), but not c-Jun N-terminal kinase (JNK), dephos-phorylation. Conversely, withdrawal of endogenous NGF was followed by p38 MAPK activation and translo-cation onto mitochondria, whereby it combined with and phosphorylated Bcl-2, as assessed by co-immuno-precipitation and kinase assays in vivo and in vitro. Mitochondria isolated from human memory B cells, then exposed to recombinant p38 MAPK, released cyto-chrome c, as did mitochondria from Bcl-2-negative MDCK cells loaded with recombinant Bcl-2. Apoptosis induced by NGF neutralization could be blocked by the specific p38 MAPK inhibitor SB203580 or by Bcl-2 mutations in Ser-87 or Thr-56. These data demonstrate that the molecular mechanisms underlying the survival factor function of NGF critically rely upon the continuous inactivation of p38 MAPK, a Bcl-2-modifying enzyme.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7ccc9cbe64342332a85320bbda483667" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945704,"asset_id":36060116,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945704/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060116"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060116"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060116; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060116]").text(description); $(".js-view-count[data-work-id=36060116]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060116; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060116']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060116, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "7ccc9cbe64342332a85320bbda483667" } } $('.js-work-strip[data-work-id=36060116]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060116,"title":"Nerve Growth Factor Inhibits Apoptosis in Memory B Lymphocytes via Inactivation of p38 MAPK, Prevention of Bcl-2 Phosphorylation, and Cytochrome c Release","translated_title":"","metadata":{"abstract":"Survival of memory B lymphocytes is tightly linked to the integrity of the Bcl-2 protein and is regulated by a nerve growth factor (NGF) autocrine circuit. In factor-starved memory B cells, the addition of exogenous NGF promptly induced p38 mitogen-activated protein kinase (MAPK), but not c-Jun N-terminal kinase (JNK), dephos-phorylation. Conversely, withdrawal of endogenous NGF was followed by p38 MAPK activation and translo-cation onto mitochondria, whereby it combined with and phosphorylated Bcl-2, as assessed by co-immuno-precipitation and kinase assays in vivo and in vitro. Mitochondria isolated from human memory B cells, then exposed to recombinant p38 MAPK, released cyto-chrome c, as did mitochondria from Bcl-2-negative MDCK cells loaded with recombinant Bcl-2. Apoptosis induced by NGF neutralization could be blocked by the specific p38 MAPK inhibitor SB203580 or by Bcl-2 mutations in Ser-87 or Thr-56. These data demonstrate that the molecular mechanisms underlying the survival factor function of NGF critically rely upon the continuous inactivation of p38 MAPK, a Bcl-2-modifying enzyme."},"translated_abstract":"Survival of memory B lymphocytes is tightly linked to the integrity of the Bcl-2 protein and is regulated by a nerve growth factor (NGF) autocrine circuit. In factor-starved memory B cells, the addition of exogenous NGF promptly induced p38 mitogen-activated protein kinase (MAPK), but not c-Jun N-terminal kinase (JNK), dephos-phorylation. Conversely, withdrawal of endogenous NGF was followed by p38 MAPK activation and translo-cation onto mitochondria, whereby it combined with and phosphorylated Bcl-2, as assessed by co-immuno-precipitation and kinase assays in vivo and in vitro. Mitochondria isolated from human memory B cells, then exposed to recombinant p38 MAPK, released cyto-chrome c, as did mitochondria from Bcl-2-negative MDCK cells loaded with recombinant Bcl-2. Apoptosis induced by NGF neutralization could be blocked by the specific p38 MAPK inhibitor SB203580 or by Bcl-2 mutations in Ser-87 or Thr-56. These data demonstrate that the molecular mechanisms underlying the survival factor function of NGF critically rely upon the continuous inactivation of p38 MAPK, a Bcl-2-modifying enzyme.","internal_url":"https://www.academia.edu/36060116/Nerve_Growth_Factor_Inhibits_Apoptosis_in_Memory_B_Lymphocytes_via_Inactivation_of_p38_MAPK_Prevention_of_Bcl_2_Phosphorylation_and_Cytochrome_c_Release","translated_internal_url":"","created_at":"2018-03-02T06:46:58.304-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136956,"work_id":36060116,"tagging_user_id":32025990,"tagged_user_id":35756305,"co_author_invite_id":null,"email":"l***i@uniroma1.it","affiliation":"Università degli Studi \"La Sapienza\" di Roma","display_order":1,"name":"Lucia Nencioni","title":"Nerve Growth Factor Inhibits Apoptosis in Memory B Lymphocytes via Inactivation of p38 MAPK, Prevention of Bcl-2 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="3019435" id="papers"><div class="js-work-strip profile--work_container" data-work-id="36060222"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060222/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases"><img alt="Research paper thumbnail of Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases" class="work-thumbnail" src="https://attachments.academia-assets.com/55945840/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060222/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases">Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/EPerissi">Eloisa Perissi</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. On the whole, our data suggest that the change in capsular phenotype may help bacterial cells of clade I to partially escape innate immune recognition and IL-1β-mediated inflammation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="a2367482ea7035f0d7b7de7bf5f4a4f1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945840,"asset_id":36060222,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945840/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060222"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060222"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060222; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060222]").text(description); $(".js-view-count[data-work-id=36060222]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060222; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060222']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060222, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "a2367482ea7035f0d7b7de7bf5f4a4f1" } } $('.js-work-strip[data-work-id=36060222]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060222,"title":"Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases","translated_title":"","metadata":{"abstract":"ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. On the whole, our data suggest that the change in capsular phenotype may help bacterial cells of clade I to partially escape innate immune recognition and IL-1β-mediated inflammation."},"translated_abstract":"ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060262"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060262/Effects_of_soluble_extracts_from_Leishmania_infantum_promastigotes_Toxoplasma_gondii_tachyzoites_on_TGF_b_mediated_pathways_in_activated_CD4_%C3%BE_T_lymphocytes"><img alt="Research paper thumbnail of Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes" class="work-thumbnail" src="https://attachments.academia-assets.com/55945878/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060262/Effects_of_soluble_extracts_from_Leishmania_infantum_promastigotes_Toxoplasma_gondii_tachyzoites_on_TGF_b_mediated_pathways_in_activated_CD4_%C3%BE_T_lymphocytes">Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/EPerissi">Eloisa Perissi</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Interference with transforming growth factor-b-mediated pathways helps several parasites to survi...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7b98a5f29cf66c0e2db5728cd782b57e" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945878,"asset_id":36060262,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945878/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060262"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060262"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060262; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060262]").text(description); $(".js-view-count[data-work-id=36060262]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060262; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060262']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060262, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "7b98a5f29cf66c0e2db5728cd782b57e" } } $('.js-work-strip[data-work-id=36060262]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060262,"title":"Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes","translated_title":"","metadata":{"abstract":"Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells."},"translated_abstract":"Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059604"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059604/Bridging_pro_inflammatory_signals_synaptic_transmission_and_protection_in_spinal_explants_in_vitro"><img alt="Research paper thumbnail of Bridging pro-inflammatory signals, synaptic transmission and protection in spinal explants in vitro" class="work-thumbnail" src="https://attachments.academia-assets.com/55945115/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059604/Bridging_pro_inflammatory_signals_synaptic_transmission_and_protection_in_spinal_explants_in_vitro">Bridging pro-inflammatory signals, synaptic transmission and protection in spinal explants in vitro</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Multiple sclerosis is characterized by tissue atrophy involving the brain and the spinal cord, wh...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Multiple sclerosis is characterized by tissue atrophy involving the brain and the spinal cord, where reactive inflammation contributes to the neurodegenerative processes. Recently, the presence of synapse alterations induced by the inflammatory responses was suggested by experimental and clinical observations, in experimental autoimmune encephalomyelitis mouse model and in patients, respectively. Further knowledge on the interplay between pro-inflammatory agents, neuroglia and synaptic dysfunction is crucial to the design of unconventional protective molecules. Here we report the effects, on spinal cord circuits, of a cytokine cocktail that partly mimics the signature of T lymphocytes sub population Th1. In embryonic mouse spinal organ-cultures, containing neuronal cells and neuroglia, cytokines induced inflammatory responses accompanied by a significant increase in spontaneous synaptic activity. We suggest that cytokines specifically altered signal integration in spinal networks by speeding the decay of GABA A responses. This hypothesis is supported by the finding that synapse protection by a non-peptidic NGF mimetic molecule prevented both the changes in the time course of GABA events and in network activity that were left unchanged by the cytokine production from astrocytes and microglia present in the cultured tissue. In conclusion, we developed an important tool for the study of synaptic alterations induced by inflammation, that takes into account the role of neuronal and not neuronal resident cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="20cff893dd9ed9c1cfb98c741df5da00" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945115,"asset_id":36059604,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945115/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059604"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059604"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059604; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059604]").text(description); $(".js-view-count[data-work-id=36059604]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059604; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059604']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059604, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "20cff893dd9ed9c1cfb98c741df5da00" } } $('.js-work-strip[data-work-id=36059604]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059604,"title":"Bridging pro-inflammatory signals, synaptic transmission and protection in spinal explants in vitro","translated_title":"","metadata":{"abstract":"Multiple sclerosis is characterized by tissue atrophy involving the brain and the spinal cord, where reactive inflammation contributes to the neurodegenerative processes. Recently, the presence of synapse alterations induced by the inflammatory responses was suggested by experimental and clinical observations, in experimental autoimmune encephalomyelitis mouse model and in patients, respectively. Further knowledge on the interplay between pro-inflammatory agents, neuroglia and synaptic dysfunction is crucial to the design of unconventional protective molecules. Here we report the effects, on spinal cord circuits, of a cytokine cocktail that partly mimics the signature of T lymphocytes sub population Th1. In embryonic mouse spinal organ-cultures, containing neuronal cells and neuroglia, cytokines induced inflammatory responses accompanied by a significant increase in spontaneous synaptic activity. We suggest that cytokines specifically altered signal integration in spinal networks by speeding the decay of GABA A responses. This hypothesis is supported by the finding that synapse protection by a non-peptidic NGF mimetic molecule prevented both the changes in the time course of GABA events and in network activity that were left unchanged by the cytokine production from astrocytes and microglia present in the cultured tissue. In conclusion, we developed an important tool for the study of synaptic alterations induced by inflammation, that takes into account the role of neuronal and not neuronal resident cells."},"translated_abstract":"Multiple sclerosis is characterized by tissue atrophy involving the brain and the spinal cord, where reactive inflammation contributes to the neurodegenerative processes. Recently, the presence of synapse alterations induced by the inflammatory responses was suggested by experimental and clinical observations, in experimental autoimmune encephalomyelitis mouse model and in patients, respectively. Further knowledge on the interplay between pro-inflammatory agents, neuroglia and synaptic dysfunction is crucial to the design of unconventional protective molecules. Here we report the effects, on spinal cord circuits, of a cytokine cocktail that partly mimics the signature of T lymphocytes sub population Th1. In embryonic mouse spinal organ-cultures, containing neuronal cells and neuroglia, cytokines induced inflammatory responses accompanied by a significant increase in spontaneous synaptic activity. We suggest that cytokines specifically altered signal integration in spinal networks by speeding the decay of GABA A responses. This hypothesis is supported by the finding that synapse protection by a non-peptidic NGF mimetic molecule prevented both the changes in the time course of GABA events and in network activity that were left unchanged by the cytokine production from astrocytes and microglia present in the cultured tissue. In conclusion, we developed an important tool for the study of synaptic alterations induced by inflammation, that takes into account the role of neuronal and not neuronal resident cells.","internal_url":"https://www.academia.edu/36059604/Bridging_pro_inflammatory_signals_synaptic_transmission_and_protection_in_spinal_explants_in_vitro","translated_internal_url":"","created_at":"2018-03-02T05:36:28.613-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136561,"work_id":36059604,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Bridging pro-inflammatory signals, synaptic transmission and protection in spinal explants in vitro"}],"downloadable_attachments":[{"id":55945115,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945115/thumbnails/1.jpg","file_name":"Bridging_pro-inflammatory_signals__synaptic.pdf","download_url":"https://www.academia.edu/attachments/55945115/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Bridging_pro_inflammatory_signals_synapt.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945115/Bridging_pro-inflammatory_signals__synaptic-libre.pdf?1519998791=\u0026response-content-disposition=attachment%3B+filename%3DBridging_pro_inflammatory_signals_synapt.pdf\u0026Expires=1732404749\u0026Signature=V04KAfctg9seCaQHBxk-2SCRfxxMATnK3FLhXtWIkdDu9vKYw4llYtXH2YAkpYcaR~R~Eg1K7h53zV3Z069g-PHNccwLObBLlQs0jHZyEZIF9iv~sRRzOPEG59rcD5SdrQ984V3Mu2nUEDjqXskvRzX-OmlKw2bC9WHn5Qb1ZbYtLXI2b9AxNhXqzpUXhCqXW9HP45MQ2Nv1wNl4YaCfZOkdgmBu2B7EaCdHApbk~9jKxPA5VWvTyYUPf3asFR3Sa8m0cRtAxrcD2wXWHadUIgXPbBGIuA4qxPdgEMJMWKldG4SObI0qu2dti5F6xrjP-vein9kuFlY4mpp3Pwrcjw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Bridging_pro_inflammatory_signals_synaptic_transmission_and_protection_in_spinal_explants_in_vitro","translated_slug":"","page_count":14,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945115,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945115/thumbnails/1.jpg","file_name":"Bridging_pro-inflammatory_signals__synaptic.pdf","download_url":"https://www.academia.edu/attachments/55945115/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Bridging_pro_inflammatory_signals_synapt.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945115/Bridging_pro-inflammatory_signals__synaptic-libre.pdf?1519998791=\u0026response-content-disposition=attachment%3B+filename%3DBridging_pro_inflammatory_signals_synapt.pdf\u0026Expires=1732404749\u0026Signature=V04KAfctg9seCaQHBxk-2SCRfxxMATnK3FLhXtWIkdDu9vKYw4llYtXH2YAkpYcaR~R~Eg1K7h53zV3Z069g-PHNccwLObBLlQs0jHZyEZIF9iv~sRRzOPEG59rcD5SdrQ984V3Mu2nUEDjqXskvRzX-OmlKw2bC9WHn5Qb1ZbYtLXI2b9AxNhXqzpUXhCqXW9HP45MQ2Nv1wNl4YaCfZOkdgmBu2B7EaCdHApbk~9jKxPA5VWvTyYUPf3asFR3Sa8m0cRtAxrcD2wXWHadUIgXPbBGIuA4qxPdgEMJMWKldG4SObI0qu2dti5F6xrjP-vein9kuFlY4mpp3Pwrcjw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":3097,"name":"Multiple sclerosis","url":"https://www.academia.edu/Documents/in/Multiple_sclerosis"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059619"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059619/Characterization_of_cervico_vaginal_microbiota_in_women_developing_persistent_high_risk_Human_Papillomavirus_infection"><img alt="Research paper thumbnail of Characterization of cervico-vaginal microbiota in women developing persistent high-risk Human Papillomavirus infection" class="work-thumbnail" src="https://attachments.academia-assets.com/55945126/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059619/Characterization_of_cervico_vaginal_microbiota_in_women_developing_persistent_high_risk_Human_Papillomavirus_infection">Characterization of cervico-vaginal microbiota in women developing persistent high-risk Human Papillomavirus infection</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Changes in cervico-vaginal microbiota with Lactobacillus depletion and increased microbial divers...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Changes in cervico-vaginal microbiota with Lactobacillus depletion and increased microbial diversity facilitate human papillomavirus (HPV) infection and might be involved in viral persistence and cancer development. To define the microbial Community State Types (CSTs) associated with high-risk HPV− persistence, we analysed 55 cervico-vaginal samples from HPV positive (HPV+) women out of 1029 screened women and performed pyrosequencing of 16S rDNA. A total of 17 samples from age-matched HPV negative (HPV−) women were used as control. Clearance or Persistence groups were defined by recalling women after one year for HPV screening and genotyping. A CST IV subgroup, with bacterial genera such as Gardnerella, Prevotella, Megasphoera, Atopobium, frequently associated with anaerobic consortium in bacterial vaginosis (BV), was present at baseline sampling in 43% of women in Persistence group, and only in 7.4% of women in Clearance group. Atopobium genus was significantly enriched in Persistence group compared to the other groups. Sialidase-encoding gene from Gardnerella vaginalis, involved in biofilm formation, was significantly more represented in Persistence group compared to the other groups. Based on these data, we consider the CST IV-BV as a risk factor for HPV persistence and we propose Atopobium spp and sialidase gene from G. vaginalis as microbial markers of HPV− persistence. Cervical cancer (CC) is one of the most common cancer in women, with an estimated incidence of 485 000 new cases and 236 000 deaths in 2013 1 , causing 6.9 million disability-adjusted life-years (DALYs). Persistence of onco-genic human papillomavirus (HPV) infection contribute to the development of CC. While the virus is cleared in more than 90% of infections within 6–18 months 2–4 , viral persistence occurs in almost 10% of infected women. The factors responsible of persistence, as well those that promote and initiate the carcinogenesis process, need to be fully elucidated. Many other factors such as immunodeficiency, age, smoking, oral contraceptives and Chlamydia trachomatis infection are related with higher persistence rates 5, 6. Recently, several scientific reports indicated the role of vaginal microbiota in the acquisition and persistence of HPV and risk of CC development 7. In the majority of human body sites, highly diverse microbial communities are generally considered a signature of health 8, 9. However, in the vaginal environment, health is commonly associated with low microbial diversity and prevalence of only a few species of Lactobacillus 10–13. Lactobacillus spp. prevent colonization of exogenous pathogens by producing lactic acid, bacteriocins and reactive oxygen species (ROS), and compete with them for Published: xx xx xxxx OPEN</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f93e76508674e5161bfc9aca846be6c4" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945126,"asset_id":36059619,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945126/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059619"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059619"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059619; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059619]").text(description); $(".js-view-count[data-work-id=36059619]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059619; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059619']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059619, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "f93e76508674e5161bfc9aca846be6c4" } } $('.js-work-strip[data-work-id=36059619]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059619,"title":"Characterization of cervico-vaginal microbiota in women developing persistent high-risk Human Papillomavirus infection","translated_title":"","metadata":{"abstract":"Changes in cervico-vaginal microbiota with Lactobacillus depletion and increased microbial diversity facilitate human papillomavirus (HPV) infection and might be involved in viral persistence and cancer development. To define the microbial Community State Types (CSTs) associated with high-risk HPV− persistence, we analysed 55 cervico-vaginal samples from HPV positive (HPV+) women out of 1029 screened women and performed pyrosequencing of 16S rDNA. A total of 17 samples from age-matched HPV negative (HPV−) women were used as control. Clearance or Persistence groups were defined by recalling women after one year for HPV screening and genotyping. A CST IV subgroup, with bacterial genera such as Gardnerella, Prevotella, Megasphoera, Atopobium, frequently associated with anaerobic consortium in bacterial vaginosis (BV), was present at baseline sampling in 43% of women in Persistence group, and only in 7.4% of women in Clearance group. Atopobium genus was significantly enriched in Persistence group compared to the other groups. Sialidase-encoding gene from Gardnerella vaginalis, involved in biofilm formation, was significantly more represented in Persistence group compared to the other groups. Based on these data, we consider the CST IV-BV as a risk factor for HPV persistence and we propose Atopobium spp and sialidase gene from G. vaginalis as microbial markers of HPV− persistence. Cervical cancer (CC) is one of the most common cancer in women, with an estimated incidence of 485 000 new cases and 236 000 deaths in 2013 1 , causing 6.9 million disability-adjusted life-years (DALYs). Persistence of onco-genic human papillomavirus (HPV) infection contribute to the development of CC. While the virus is cleared in more than 90% of infections within 6–18 months 2–4 , viral persistence occurs in almost 10% of infected women. The factors responsible of persistence, as well those that promote and initiate the carcinogenesis process, need to be fully elucidated. Many other factors such as immunodeficiency, age, smoking, oral contraceptives and Chlamydia trachomatis infection are related with higher persistence rates 5, 6. Recently, several scientific reports indicated the role of vaginal microbiota in the acquisition and persistence of HPV and risk of CC development 7. In the majority of human body sites, highly diverse microbial communities are generally considered a signature of health 8, 9. However, in the vaginal environment, health is commonly associated with low microbial diversity and prevalence of only a few species of Lactobacillus 10–13. Lactobacillus spp. prevent colonization of exogenous pathogens by producing lactic acid, bacteriocins and reactive oxygen species (ROS), and compete with them for Published: xx xx xxxx OPEN"},"translated_abstract":"Changes in cervico-vaginal microbiota with Lactobacillus depletion and increased microbial diversity facilitate human papillomavirus (HPV) infection and might be involved in viral persistence and cancer development. To define the microbial Community State Types (CSTs) associated with high-risk HPV− persistence, we analysed 55 cervico-vaginal samples from HPV positive (HPV+) women out of 1029 screened women and performed pyrosequencing of 16S rDNA. A total of 17 samples from age-matched HPV negative (HPV−) women were used as control. Clearance or Persistence groups were defined by recalling women after one year for HPV screening and genotyping. A CST IV subgroup, with bacterial genera such as Gardnerella, Prevotella, Megasphoera, Atopobium, frequently associated with anaerobic consortium in bacterial vaginosis (BV), was present at baseline sampling in 43% of women in Persistence group, and only in 7.4% of women in Clearance group. Atopobium genus was significantly enriched in Persistence group compared to the other groups. Sialidase-encoding gene from Gardnerella vaginalis, involved in biofilm formation, was significantly more represented in Persistence group compared to the other groups. Based on these data, we consider the CST IV-BV as a risk factor for HPV persistence and we propose Atopobium spp and sialidase gene from G. vaginalis as microbial markers of HPV− persistence. Cervical cancer (CC) is one of the most common cancer in women, with an estimated incidence of 485 000 new cases and 236 000 deaths in 2013 1 , causing 6.9 million disability-adjusted life-years (DALYs). Persistence of onco-genic human papillomavirus (HPV) infection contribute to the development of CC. While the virus is cleared in more than 90% of infections within 6–18 months 2–4 , viral persistence occurs in almost 10% of infected women. The factors responsible of persistence, as well those that promote and initiate the carcinogenesis process, need to be fully elucidated. Many other factors such as immunodeficiency, age, smoking, oral contraceptives and Chlamydia trachomatis infection are related with higher persistence rates 5, 6. Recently, several scientific reports indicated the role of vaginal microbiota in the acquisition and persistence of HPV and risk of CC development 7. In the majority of human body sites, highly diverse microbial communities are generally considered a signature of health 8, 9. However, in the vaginal environment, health is commonly associated with low microbial diversity and prevalence of only a few species of Lactobacillus 10–13. Lactobacillus spp. prevent colonization of exogenous pathogens by producing lactic acid, bacteriocins and reactive oxygen species (ROS), and compete with them for Published: xx xx xxxx OPEN","internal_url":"https://www.academia.edu/36059619/Characterization_of_cervico_vaginal_microbiota_in_women_developing_persistent_high_risk_Human_Papillomavirus_infection","translated_internal_url":"","created_at":"2018-03-02T05:38:19.144-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136565,"work_id":36059619,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Characterization of cervico-vaginal microbiota in women developing persistent high-risk Human Papillomavirus infection"}],"downloadable_attachments":[{"id":55945126,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945126/thumbnails/1.jpg","file_name":"Characterization_of_cervico-vaginal_microbiota_in_women_developing_persistent_high-risk_Human_Papillomavirus_infection.pdf","download_url":"https://www.academia.edu/attachments/55945126/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Characterization_of_cervico_vaginal_micr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945126/Characterization_of_cervico-vaginal_microbiota_in_women_developing_persistent_high-risk_Human_Papillomavirus_infection-libre.pdf?1519998785=\u0026response-content-disposition=attachment%3B+filename%3DCharacterization_of_cervico_vaginal_micr.pdf\u0026Expires=1732263172\u0026Signature=K7O-HPlJWnOkMcGtvMqQDJtGTXwxU2QOSFohQX7~X2GM5wnnsOHrNzxWp00a5cpZIdJfKgoW6yl4WTY0~oAYVh~n13MKW4lu~42SlJZxs6CD9BcfVPKE8i-ZzBnAZF01ywWxfJa5-yIe2uPrXih0YuCAq9jCb-qCeao~TdwH~3gcie9fIvdCp8Ze1g7djmLGmyttF4MrRb8JEED~Gxxva83qmtKKsNIChCLascr4RCZV6bTpuuys1rGrRcdaIRAvvzYMLip03IhFrjYo6LXWvh~FwqEGWTs8xx6qxrsyYKpw-DiIbgn6WBXtzD1heTTrlGq~h8mFVlbaMWBzoQ1V9A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Characterization_of_cervico_vaginal_microbiota_in_women_developing_persistent_high_risk_Human_Papillomavirus_infection","translated_slug":"","page_count":12,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945126,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945126/thumbnails/1.jpg","file_name":"Characterization_of_cervico-vaginal_microbiota_in_women_developing_persistent_high-risk_Human_Papillomavirus_infection.pdf","download_url":"https://www.academia.edu/attachments/55945126/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Characterization_of_cervico_vaginal_micr.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945126/Characterization_of_cervico-vaginal_microbiota_in_women_developing_persistent_high-risk_Human_Papillomavirus_infection-libre.pdf?1519998785=\u0026response-content-disposition=attachment%3B+filename%3DCharacterization_of_cervico_vaginal_micr.pdf\u0026Expires=1732263172\u0026Signature=K7O-HPlJWnOkMcGtvMqQDJtGTXwxU2QOSFohQX7~X2GM5wnnsOHrNzxWp00a5cpZIdJfKgoW6yl4WTY0~oAYVh~n13MKW4lu~42SlJZxs6CD9BcfVPKE8i-ZzBnAZF01ywWxfJa5-yIe2uPrXih0YuCAq9jCb-qCeao~TdwH~3gcie9fIvdCp8Ze1g7djmLGmyttF4MrRb8JEED~Gxxva83qmtKKsNIChCLascr4RCZV6bTpuuys1rGrRcdaIRAvvzYMLip03IhFrjYo6LXWvh~FwqEGWTs8xx6qxrsyYKpw-DiIbgn6WBXtzD1heTTrlGq~h8mFVlbaMWBzoQ1V9A__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":173523,"name":"HPV","url":"https://www.academia.edu/Documents/in/HPV"},{"id":203512,"name":"Cervical Cancer","url":"https://www.academia.edu/Documents/in/Cervical_Cancer"},{"id":465741,"name":"Vaginal Microbiota","url":"https://www.academia.edu/Documents/in/Vaginal_Microbiota"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059652"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059652/Differential_Th17_response_induced_by_the_two_clades_of_the_pandemic_ST258_Klebsiella_pneumoniae_clonal_lineages_producing_KPC_type_carbapenemase"><img alt="Research paper thumbnail of Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC- type carbapenemase" class="work-thumbnail" src="https://attachments.academia-assets.com/55945151/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059652/Differential_Th17_response_induced_by_the_two_clades_of_the_pandemic_ST258_Klebsiella_pneumoniae_clonal_lineages_producing_KPC_type_carbapenemase">Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC- type carbapenemase</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The spread of KPC-type carbapenemases is mainly attributed to the global dissemination of Klebsie...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The spread of KPC-type carbapenemases is mainly attributed to the global dissemination of Klebsiella pneumoniae (KP) strains belonging to the clonal group (CG) 258, including sequence type (ST) 258 and other related STs. Two distinct clades of CG258-KP have evolved, which differ mainly for the composition of their capsular polysaccharides, and recent studies indicate that clade 1 evolved from an ancestor of clade 2 by recombination of a genomic fragment carrying the capsular polysaccharide (cps) locus. In this paper, we investigated the ability of two ST258-KP strains, KKBO-1 and KK207-1, selected as representatives of ST258-KP clade 2 and clade 1, respectively, to activate an adaptive immune response using ex vivo-stimulation of PBMC from normal donors as an experimental model. Our data showed that KKBO-1 (clade 2) induces a Th17 response more efficiently than KK207-1 (clade 1): the percentage of CD4 + IL17 + cells and the production of IL-17A were significantly higher in cultures with KKBO-1 compared to cultures with KK207-1. While no differences in the rate of bacterial internalization or in the bacteria-induced expression of CD86 and HLA-DR by monocytes and myeloid dendritic cells were revealed, we found that the two strains significantly differ in inducing the production of cytokines involved in the adaptive immune response, as IL-1β, IL-23 and TNF-α, by antigen-presenting cells, with KKBO-1 being a more efficient inducer than KK207-1. The immune responses elicited by KK207-1 were comparable to those elicited by CIP 52.145, a highly virulent K. pneumoniae reference strain known to escape immune-inflammatory responses. Altogether, present results suggest that CG258-KP of the two clades are capable of inducing a different response of adaptive immunity in the human host.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="778924d6aa0552240b3936bccd481a18" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945151,"asset_id":36059652,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945151/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059652"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059652"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059652; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059652]").text(description); $(".js-view-count[data-work-id=36059652]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059652; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059652']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059652, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "778924d6aa0552240b3936bccd481a18" } } $('.js-work-strip[data-work-id=36059652]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059652,"title":"Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC- type carbapenemase","translated_title":"","metadata":{"abstract":"The spread of KPC-type carbapenemases is mainly attributed to the global dissemination of Klebsiella pneumoniae (KP) strains belonging to the clonal group (CG) 258, including sequence type (ST) 258 and other related STs. Two distinct clades of CG258-KP have evolved, which differ mainly for the composition of their capsular polysaccharides, and recent studies indicate that clade 1 evolved from an ancestor of clade 2 by recombination of a genomic fragment carrying the capsular polysaccharide (cps) locus. In this paper, we investigated the ability of two ST258-KP strains, KKBO-1 and KK207-1, selected as representatives of ST258-KP clade 2 and clade 1, respectively, to activate an adaptive immune response using ex vivo-stimulation of PBMC from normal donors as an experimental model. Our data showed that KKBO-1 (clade 2) induces a Th17 response more efficiently than KK207-1 (clade 1): the percentage of CD4 + IL17 + cells and the production of IL-17A were significantly higher in cultures with KKBO-1 compared to cultures with KK207-1. While no differences in the rate of bacterial internalization or in the bacteria-induced expression of CD86 and HLA-DR by monocytes and myeloid dendritic cells were revealed, we found that the two strains significantly differ in inducing the production of cytokines involved in the adaptive immune response, as IL-1β, IL-23 and TNF-α, by antigen-presenting cells, with KKBO-1 being a more efficient inducer than KK207-1. The immune responses elicited by KK207-1 were comparable to those elicited by CIP 52.145, a highly virulent K. pneumoniae reference strain known to escape immune-inflammatory responses. Altogether, present results suggest that CG258-KP of the two clades are capable of inducing a different response of adaptive immunity in the human host."},"translated_abstract":"The spread of KPC-type carbapenemases is mainly attributed to the global dissemination of Klebsiella pneumoniae (KP) strains belonging to the clonal group (CG) 258, including sequence type (ST) 258 and other related STs. Two distinct clades of CG258-KP have evolved, which differ mainly for the composition of their capsular polysaccharides, and recent studies indicate that clade 1 evolved from an ancestor of clade 2 by recombination of a genomic fragment carrying the capsular polysaccharide (cps) locus. In this paper, we investigated the ability of two ST258-KP strains, KKBO-1 and KK207-1, selected as representatives of ST258-KP clade 2 and clade 1, respectively, to activate an adaptive immune response using ex vivo-stimulation of PBMC from normal donors as an experimental model. Our data showed that KKBO-1 (clade 2) induces a Th17 response more efficiently than KK207-1 (clade 1): the percentage of CD4 + IL17 + cells and the production of IL-17A were significantly higher in cultures with KKBO-1 compared to cultures with KK207-1. While no differences in the rate of bacterial internalization or in the bacteria-induced expression of CD86 and HLA-DR by monocytes and myeloid dendritic cells were revealed, we found that the two strains significantly differ in inducing the production of cytokines involved in the adaptive immune response, as IL-1β, IL-23 and TNF-α, by antigen-presenting cells, with KKBO-1 being a more efficient inducer than KK207-1. The immune responses elicited by KK207-1 were comparable to those elicited by CIP 52.145, a highly virulent K. pneumoniae reference strain known to escape immune-inflammatory responses. Altogether, present results suggest that CG258-KP of the two clades are capable of inducing a different response of adaptive immunity in the human host.","internal_url":"https://www.academia.edu/36059652/Differential_Th17_response_induced_by_the_two_clades_of_the_pandemic_ST258_Klebsiella_pneumoniae_clonal_lineages_producing_KPC_type_carbapenemase","translated_internal_url":"","created_at":"2018-03-02T05:44:16.874-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136578,"work_id":36059652,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC- type carbapenemase"},{"id":31136579,"work_id":36059652,"tagging_user_id":32025990,"tagged_user_id":32025990,"co_author_invite_id":6640218,"email":"m***a@unifi.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":2,"name":"Maria Gabriella Torcia","title":"Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC- type carbapenemase"},{"id":31136580,"work_id":36059652,"tagging_user_id":32025990,"tagged_user_id":32099627,"co_author_invite_id":null,"email":"m***i@unifi.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":3,"name":"Michele Tanturli","title":"Differential Th17 response induced by the two clades of the pandemic ST258 Klebsiella pneumoniae clonal lineages producing KPC- type carbapenemase"}],"downloadable_attachments":[{"id":55945151,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945151/thumbnails/1.jpg","file_name":"Differential_Th17_response_induced_by_the.pdf","download_url":"https://www.academia.edu/attachments/55945151/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Differential_Th17_response_induced_by_th.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945151/Differential_Th17_response_induced_by_the-libre.pdf?1519998765=\u0026response-content-disposition=attachment%3B+filename%3DDifferential_Th17_response_induced_by_th.pdf\u0026Expires=1732404749\u0026Signature=QUB5RgA7aSmNYf9wHhqvJW5a9x9Txb5BN3MnE3sD7gdksnd3hGGgWebudo9gdOuDSu5P9djMRBKfKXchbmXkzpAAHRKgdNCw8dB5aPxsUw3XGPivcQxmgRmlnzBsCefGCP5rA-DvvJ4qlWtByC7CFbRW-ek9FqxcE--NR-NA-NA7sLYGu~Z1aVG0dRyGJhVBm1MaeU1lm0z84vaQFM4jxua3lgL4Rz2U~Wz~U8x2zU6GKpC75qwTbMNHMcwvlYyi-kFA6waTJ67l5FR6eIsvzbUHuHdr0yVc1xPEohc3JZBoqgr4dEtGs7AbVZoAp51iR1yB0wWZ0u94Eh9yzkNjHw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Differential_Th17_response_induced_by_the_two_clades_of_the_pandemic_ST258_Klebsiella_pneumoniae_clonal_lineages_producing_KPC_type_carbapenemase","translated_slug":"","page_count":15,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945151,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945151/thumbnails/1.jpg","file_name":"Differential_Th17_response_induced_by_the.pdf","download_url":"https://www.academia.edu/attachments/55945151/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Differential_Th17_response_induced_by_th.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945151/Differential_Th17_response_induced_by_the-libre.pdf?1519998765=\u0026response-content-disposition=attachment%3B+filename%3DDifferential_Th17_response_induced_by_th.pdf\u0026Expires=1732404749\u0026Signature=QUB5RgA7aSmNYf9wHhqvJW5a9x9Txb5BN3MnE3sD7gdksnd3hGGgWebudo9gdOuDSu5P9djMRBKfKXchbmXkzpAAHRKgdNCw8dB5aPxsUw3XGPivcQxmgRmlnzBsCefGCP5rA-DvvJ4qlWtByC7CFbRW-ek9FqxcE--NR-NA-NA7sLYGu~Z1aVG0dRyGJhVBm1MaeU1lm0z84vaQFM4jxua3lgL4Rz2U~Wz~U8x2zU6GKpC75qwTbMNHMcwvlYyi-kFA6waTJ67l5FR6eIsvzbUHuHdr0yVc1xPEohc3JZBoqgr4dEtGs7AbVZoAp51iR1yB0wWZ0u94Eh9yzkNjHw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":112322,"name":"Klebsiella","url":"https://www.academia.edu/Documents/in/Klebsiella"},{"id":1764389,"name":"KPC-2-Producing Klebsiella pneumoniae","url":"https://www.academia.edu/Documents/in/KPC-2-Producing_Klebsiella_pneumoniae"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059681"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059681/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes"><img alt="Research paper thumbnail of Crohn's Colitis: Development of a multiplex gene expression assay comparing mRNA levels of susceptibility genes" class="work-thumbnail" src="https://attachments.academia-assets.com/55945201/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059681/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes">Crohn's Colitis: Development of a multiplex gene expression assay comparing mRNA levels of susceptibility genes</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Crohn's disease (CD) is a multifactorial immunologically mediated disease. In this study we explo...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Crohn's disease (CD) is a multifactorial immunologically mediated disease. In this study we explored, for the first time, the efficacy of the Multiplex Gene Assay technology for detecting mRNA expression profile of 24 selected CD related genes in endoscopic biopsies and surgical specimens from CD patients with colonic localization of the disease. The polymorphisms of genes most frequently associated with CD were also analysed in DNA samples from the same patients. The analysis of endoscopic samples showed increased expression of 7 genes in inflamed mucosa compared to non-inflamed mucosa and suggests the activation of the autophagy process and of a Th17 adaptive response. The analysis of surgical specimens showed increased expression of 16 genes in inflamed tissue compared to non-inflamed internal controls and revealed the activation of immune-adaptive Th17 response in association with a Th1 response.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="98d3596305eca6fb3ce932edcb230d7b" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945201,"asset_id":36059681,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945201/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059681"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059681"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059681; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059681]").text(description); $(".js-view-count[data-work-id=36059681]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059681; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059681']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059681, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "98d3596305eca6fb3ce932edcb230d7b" } } $('.js-work-strip[data-work-id=36059681]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059681,"title":"Crohn's Colitis: Development of a multiplex gene expression assay comparing mRNA levels of susceptibility genes","translated_title":"","metadata":{"abstract":"Crohn's disease (CD) is a multifactorial immunologically mediated disease. In this study we explored, for the first time, the efficacy of the Multiplex Gene Assay technology for detecting mRNA expression profile of 24 selected CD related genes in endoscopic biopsies and surgical specimens from CD patients with colonic localization of the disease. The polymorphisms of genes most frequently associated with CD were also analysed in DNA samples from the same patients. The analysis of endoscopic samples showed increased expression of 7 genes in inflamed mucosa compared to non-inflamed mucosa and suggests the activation of the autophagy process and of a Th17 adaptive response. The analysis of surgical specimens showed increased expression of 16 genes in inflamed tissue compared to non-inflamed internal controls and revealed the activation of immune-adaptive Th17 response in association with a Th1 response."},"translated_abstract":"Crohn's disease (CD) is a multifactorial immunologically mediated disease. In this study we explored, for the first time, the efficacy of the Multiplex Gene Assay technology for detecting mRNA expression profile of 24 selected CD related genes in endoscopic biopsies and surgical specimens from CD patients with colonic localization of the disease. The polymorphisms of genes most frequently associated with CD were also analysed in DNA samples from the same patients. The analysis of endoscopic samples showed increased expression of 7 genes in inflamed mucosa compared to non-inflamed mucosa and suggests the activation of the autophagy process and of a Th17 adaptive response. The analysis of surgical specimens showed increased expression of 16 genes in inflamed tissue compared to non-inflamed internal controls and revealed the activation of immune-adaptive Th17 response in association with a Th1 response.","internal_url":"https://www.academia.edu/36059681/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes","translated_internal_url":"","created_at":"2018-03-02T05:47:27.816-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":55945201,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945201/thumbnails/1.jpg","file_name":"Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes.pdf","download_url":"https://www.academia.edu/attachments/55945201/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Crohns_Colitis_Development_of_a_multiple.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945201/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes-libre.pdf?1519999050=\u0026response-content-disposition=attachment%3B+filename%3DCrohns_Colitis_Development_of_a_multiple.pdf\u0026Expires=1732404749\u0026Signature=T7M7KtkGUz9dwQOLbAqZibvoXVHb6vQA-ae4-WRAVv0DL3saxjPVVKV~uuyjVfkVIuBBLARnYRfT8r1nxqObP9La-NImYOFtMAS0UJfRmAg9jQIUN8JZ64AYXZiVtmWsj25BJDtyp0qFocAAmPOiRLTt0XJT9efQx0Ib7j9Yi7BdVm22qYP39vEkGD79hMrNwSsSNNbPL-1UZDACaSmHhs1VCMCYh4YCvx3TLaVJZ0euRsVhEQpbvmPvNJcjsdRo71XRTR7vFFDxfwuTVP3bCm0ayjttsIKXz50TkItmxzwhOfroE5pplgSNBMk9yfQsCf1w6-KWp9y0tMmtHXawuw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes","translated_slug":"","page_count":10,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945201,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945201/thumbnails/1.jpg","file_name":"Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes.pdf","download_url":"https://www.academia.edu/attachments/55945201/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Crohns_Colitis_Development_of_a_multiple.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945201/Crohns_Colitis_Development_of_a_multiplex_gene_expression_assay_comparing_mRNA_levels_of_susceptibility_genes-libre.pdf?1519999050=\u0026response-content-disposition=attachment%3B+filename%3DCrohns_Colitis_Development_of_a_multiple.pdf\u0026Expires=1732404749\u0026Signature=T7M7KtkGUz9dwQOLbAqZibvoXVHb6vQA-ae4-WRAVv0DL3saxjPVVKV~uuyjVfkVIuBBLARnYRfT8r1nxqObP9La-NImYOFtMAS0UJfRmAg9jQIUN8JZ64AYXZiVtmWsj25BJDtyp0qFocAAmPOiRLTt0XJT9efQx0Ib7j9Yi7BdVm22qYP39vEkGD79hMrNwSsSNNbPL-1UZDACaSmHhs1VCMCYh4YCvx3TLaVJZ0euRsVhEQpbvmPvNJcjsdRo71XRTR7vFFDxfwuTVP3bCm0ayjttsIKXz50TkItmxzwhOfroE5pplgSNBMk9yfQsCf1w6-KWp9y0tMmtHXawuw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":59365,"name":"Crohn's Disease","url":"https://www.academia.edu/Documents/in/Crohns_Disease"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059703"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059703/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases"><img alt="Research paper thumbnail of Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases" class="work-thumbnail" src="https://attachments.academia-assets.com/55945221/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059703/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases">Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. On the whole, our data suggest that the change in capsular phenotype may help bacterial cells of clade I to partially escape innate immune recognition and IL-1β-mediated inflammation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="34d0c3b69a38a4d045fdbd42a9268c48" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945221,"asset_id":36059703,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945221/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059703"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059703"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059703; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059703]").text(description); $(".js-view-count[data-work-id=36059703]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059703; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059703']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059703, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "34d0c3b69a38a4d045fdbd42a9268c48" } } $('.js-work-strip[data-work-id=36059703]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059703,"title":"Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases","translated_title":"","metadata":{"abstract":"ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. On the whole, our data suggest that the change in capsular phenotype may help bacterial cells of clade I to partially escape innate immune recognition and IL-1β-mediated inflammation."},"translated_abstract":"ST258-K. pneumoniae (ST258-KP) strains, the most widespread multidrug-resistant hospital acquired pathogens, belong to at least two clades differing in a 215 Kb genomic region that includes the cluster of capsule genes. To investigate the effects of the different capsular phenotype on host-pathogen interactions, we studied representatives of ST258-KP clades, KKBO-1 and KK207-1, for their ability to activate monocytes and myeloid dendritic cells from human immune competent hosts. The two ST258-KP strains strongly induced the production of inflammatory cytokines. Significant differences between the strains were found in their ability to induce the production of IL-1β: KK207-1/clade I was much less effective than KKBO-1/clade II in inducing IL-1β production by monocytes and dendritic cells. The activation of NLRP3 inflammasome pathway by live cells and/or purified capsular polysaccharides was studied in monocytes and dendritic cells. We found that glibenclamide, a NLRP3 inhibi-tor, inhibits more than 90% of the production of mature IL-1β induced by KKBO1 and KK207-1. KK207-1 was always less efficient compared to KKBO-1 in: a) inducing NLRP3 and pro-IL-1β gene and protein expression; b) in inducing caspase-1 activation and pro-IL-1β cleavage. Capsular composition may play a role in the differential inflammatory response induced by the ST258-KP strains since capsular polysaccharides purified from bacterial cells affect NLRP3 and pro-IL-1β gene expression through p38MAPK-and NF-κB-mediated pathways. In each of these functions, capsular polysaccharides from KK207-1 were significantly less efficient compared to those purified from KKBO-1. On the whole, our data suggest that the change in capsular phenotype may help bacterial cells of clade I to partially escape innate immune recognition and IL-1β-mediated inflammation.","internal_url":"https://www.academia.edu/36059703/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases","translated_internal_url":"","created_at":"2018-03-02T05:50:46.939-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136591,"work_id":36059703,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases"},{"id":31136592,"work_id":36059703,"tagging_user_id":32025990,"tagged_user_id":32099627,"co_author_invite_id":null,"email":"m***i@unifi.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":2,"name":"Michele Tanturli","title":"Differences in Inflammatory Response Induced by Two Representatives of Clades of the Pandemic ST258 Klebsiella pneumoniae Clonal Lineage Producing KPC-Type Carbapenemases"}],"downloadable_attachments":[{"id":55945221,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945221/thumbnails/1.jpg","file_name":"Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae.pdf","download_url":"https://www.academia.edu/attachments/55945221/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Differences_in_Inflammatory_Response_Ind.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945221/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae-libre.pdf?1519999383=\u0026response-content-disposition=attachment%3B+filename%3DDifferences_in_Inflammatory_Response_Ind.pdf\u0026Expires=1732404749\u0026Signature=Mnnka6KY~fdtrzUL6sGwhMuFrlgWD5jrFc22Xg2PeWoa7qCbSlNSgVT5joHlramMuNFpcirJ1BTK65IrwKLr1c3XPxu0ul08q2h9TYkkpCkcF6hCAspFws6GKSTDWoEiBCkfuktKr03u5dlrS55kibKKd58SaOFpl8GCrl1bpEX2dPvE8rR8VyhERlLxrXzWnNwGO4ZRrTV2RFQL7V5KzbE5PiVy~f2mZ6yibhJ4c1NUEioX9yZhYYihLy0ZxMNAAJLoRDCjDGjSFecDcBXwUmFEBDPvtanDfV-hFNVa~UaNMsGjuWiF4IFyIBRHgcrG3x0t3HqepMv6I~QoMx4GUQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae_Clonal_Lineage_Producing_KPC_Type_Carbapenemases","translated_slug":"","page_count":17,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945221,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945221/thumbnails/1.jpg","file_name":"Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae.pdf","download_url":"https://www.academia.edu/attachments/55945221/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Differences_in_Inflammatory_Response_Ind.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945221/Differences_in_Inflammatory_Response_Induced_by_Two_Representatives_of_Clades_of_the_Pandemic_ST258_Klebsiella_pneumoniae-libre.pdf?1519999383=\u0026response-content-disposition=attachment%3B+filename%3DDifferences_in_Inflammatory_Response_Ind.pdf\u0026Expires=1732404749\u0026Signature=Mnnka6KY~fdtrzUL6sGwhMuFrlgWD5jrFc22Xg2PeWoa7qCbSlNSgVT5joHlramMuNFpcirJ1BTK65IrwKLr1c3XPxu0ul08q2h9TYkkpCkcF6hCAspFws6GKSTDWoEiBCkfuktKr03u5dlrS55kibKKd58SaOFpl8GCrl1bpEX2dPvE8rR8VyhERlLxrXzWnNwGO4ZRrTV2RFQL7V5KzbE5PiVy~f2mZ6yibhJ4c1NUEioX9yZhYYihLy0ZxMNAAJLoRDCjDGjSFecDcBXwUmFEBDPvtanDfV-hFNVa~UaNMsGjuWiF4IFyIBRHgcrG3x0t3HqepMv6I~QoMx4GUQ__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":112322,"name":"Klebsiella","url":"https://www.academia.edu/Documents/in/Klebsiella"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="16117323"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/16117323/Effects_of_near_infrared_laser_radiation_on_the_survival_and_inflammatory_potential_of_Candida_spp_involved_in_the_pathogenesis_of_chemotherapy_induced_oral_mucositis"><img alt="Research paper thumbnail of Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/16117323/Effects_of_near_infrared_laser_radiation_on_the_survival_and_inflammatory_potential_of_Candida_spp_involved_in_the_pathogenesis_of_chemotherapy_induced_oral_mucositis">Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MicheleTanturli">Michele Tanturli</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/LisaRizzetto">Lisa Rizzetto</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Candida spp. usually colonize ulcerative lesions of atrophic mucosa in patients with chemotherapy...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Candida spp. usually colonize ulcerative lesions of atrophic mucosa in patients with chemotherapy-induced oral mucositis inducing severe inflammation. The spread of antifungal-esistant strains strongly encouraged the search of complementary or alternative therapeutic strategies to cure inflamed mucosa. In this paper, we studied the effects of a near-infrared (NIR) laser system with dual-wavelength emission (808 nm+904 nm) on the survival and inflammatory potential of C. albicans, C. glabrata, and C. parapsilosis. Laser treatment was performed with a Multiwave Locked System laser. Survival and apoptosis of fungal strains were evaluated by colony-forming units (CFU)  counting and annexin V staining. Cytokine production was evaluated by ImmunoPlex array. Laser treatment significantly affected the survival of Candida spp. by inducing apoptosis and  induced a lower production of inflammatory cytokines by dendritic cells compared to untreated fungi. No differences in the survival and inflammatory potential were recorded in treated or untreated Saccharomyces cerevisiae cells, used as the control nonpathogenic microorganism. Laser treatment altered the survival and inflammatory potential of pathogenic Candida spp. These data provide experimental support to the use of NIR laser radiation as a co-adjuvant of antifungal therapy in patients with oral mucositis (OM) complicated by Candida infections.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="16117323"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="16117323"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 16117323; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=16117323]").text(description); $(".js-view-count[data-work-id=16117323]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 16117323; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='16117323']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 16117323, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=16117323]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":16117323,"title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis","translated_title":"","metadata":{"abstract":"Candida spp. usually colonize ulcerative lesions of atrophic mucosa in patients with chemotherapy-induced oral mucositis inducing severe inflammation. The spread of antifungal-esistant strains strongly encouraged the search of complementary or alternative therapeutic strategies to cure inflamed mucosa. In this paper, we studied the effects of a near-infrared (NIR) laser system with dual-wavelength emission (808 nm+904 nm) on the survival and inflammatory potential of C. albicans, C. glabrata, and C. parapsilosis. Laser treatment was performed with a Multiwave Locked System laser. Survival and apoptosis of fungal strains were evaluated by colony-forming units (CFU) counting and annexin V staining. Cytokine production was evaluated by ImmunoPlex array. Laser treatment significantly affected the survival of Candida spp. by inducing apoptosis and induced a lower production of inflammatory cytokines by dendritic cells compared to untreated fungi. No differences in the survival and inflammatory potential were recorded in treated or untreated Saccharomyces cerevisiae cells, used as the control nonpathogenic microorganism. Laser treatment altered the survival and inflammatory potential of pathogenic Candida spp. These data provide experimental support to the use of NIR laser radiation as a co-adjuvant of antifungal therapy in patients with oral mucositis (OM) complicated by Candida infections."},"translated_abstract":"Candida spp. usually colonize ulcerative lesions of atrophic mucosa in patients with chemotherapy-induced oral mucositis inducing severe inflammation. The spread of antifungal-esistant strains strongly encouraged the search of complementary or alternative therapeutic strategies to cure inflamed mucosa. In this paper, we studied the effects of a near-infrared (NIR) laser system with dual-wavelength emission (808 nm+904 nm) on the survival and inflammatory potential of C. albicans, C. glabrata, and C. parapsilosis. Laser treatment was performed with a Multiwave Locked System laser. Survival and apoptosis of fungal strains were evaluated by colony-forming units (CFU) counting and annexin V staining. Cytokine production was evaluated by ImmunoPlex array. Laser treatment significantly affected the survival of Candida spp. by inducing apoptosis and induced a lower production of inflammatory cytokines by dendritic cells compared to untreated fungi. No differences in the survival and inflammatory potential were recorded in treated or untreated Saccharomyces cerevisiae cells, used as the control nonpathogenic microorganism. Laser treatment altered the survival and inflammatory potential of pathogenic Candida spp. These data provide experimental support to the use of NIR laser radiation as a co-adjuvant of antifungal therapy in patients with oral mucositis (OM) complicated by Candida infections.","internal_url":"https://www.academia.edu/16117323/Effects_of_near_infrared_laser_radiation_on_the_survival_and_inflammatory_potential_of_Candida_spp_involved_in_the_pathogenesis_of_chemotherapy_induced_oral_mucositis","translated_internal_url":"","created_at":"2015-09-24T01:58:59.945-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32099627,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":6209098,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":32097049,"co_author_invite_id":null,"email":"a***e@virgilio.it","display_order":0,"name":"Annmaria Clemente","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209099,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":31719145,"co_author_invite_id":null,"email":"l***o@fmach.it","display_order":4194304,"name":"Lisa Rizzetto","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209100,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":14476117,"co_author_invite_id":null,"email":"m***w@email.it","display_order":6291456,"name":"Eloisa Perissi","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209101,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":7340032,"name":"Federico Cozzolino","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209102,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":22224088,"co_author_invite_id":null,"email":"f***i@libero.it","display_order":7864320,"name":"Franco Fusi","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":6209103,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":3382639,"co_author_invite_id":null,"email":"v***o@yahoo.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":8126464,"name":"Leonardo Vignali","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"},{"id":25071196,"work_id":16117323,"tagging_user_id":32099627,"tagged_user_id":32025990,"co_author_invite_id":null,"email":"m***a@unifi.it","affiliation":"Università degli Studi di Firenze (University of Florence)","display_order":8323072,"name":"Maria Gabriella Torcia","title":"Effects of near-infrared laser radiation on the survival and inflammatory potential of Candida spp. involved in the pathogenesis of chemotherapy-induced oral mucositis"}],"downloadable_attachments":[],"slug":"Effects_of_near_infrared_laser_radiation_on_the_survival_and_inflammatory_potential_of_Candida_spp_involved_in_the_pathogenesis_of_chemotherapy_induced_oral_mucositis","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":32099627,"first_name":"Michele","middle_initials":"","last_name":"Tanturli","page_name":"MicheleTanturli","domain_name":"unifi","created_at":"2015-06-11T07:46:56.944-07:00","display_name":"Michele Tanturli","url":"https://unifi.academia.edu/MicheleTanturli"},"attachments":[],"research_interests":[{"id":23940,"name":"Near Infrared","url":"https://www.academia.edu/Documents/in/Near_Infrared"},{"id":105582,"name":"Candida","url":"https://www.academia.edu/Documents/in/Candida"},{"id":131573,"name":"Candida albicans","url":"https://www.academia.edu/Documents/in/Candida_albicans"},{"id":335966,"name":"Candida parapsilosis","url":"https://www.academia.edu/Documents/in/Candida_parapsilosis"},{"id":550226,"name":"Oral mucositis","url":"https://www.academia.edu/Documents/in/Oral_mucositis"},{"id":1607687,"name":"Chemotherapy-induced mucositis","url":"https://www.academia.edu/Documents/in/Chemotherapy-induced_mucositis"}],"urls":[{"id":5773729,"url":"http://www.ncbi.nlm.nih.gov/pubmed/26173694"}]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059713"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059713/Effects_of_soluble_extracts_from_Leishmania_infantum_promastigotes_Toxoplasma_gondii_tachyzoites_on_TGF_b_mediated_pathways_in_activated_CD4_%C3%BE_T_lymphocytes"><img alt="Research paper thumbnail of Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes" class="work-thumbnail" src="https://attachments.academia-assets.com/55945235/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059713/Effects_of_soluble_extracts_from_Leishmania_infantum_promastigotes_Toxoplasma_gondii_tachyzoites_on_TGF_b_mediated_pathways_in_activated_CD4_%C3%BE_T_lymphocytes">Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/CSeverini1">C. Severini</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Interference with transforming growth factor-b-mediated pathways helps several parasites to survi...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. We explored the properties of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites, Trichinella spiralis muscle larvae to expand the pool of T-regulatory cells in a population of polyclonally activated T cells in the absence of accessory cells, and compared their effects to those induced by Plasmodium falciparum extracts. Similarly to P. falciparum, L. infantum extracts activate the latent soluble form of transforming growth factor-b and that bound to the membrane of activated T lymphocytes. The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="52a4ff6a09f010d0a9710ac38f9db08d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945235,"asset_id":36059713,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945235/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059713"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059713"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059713; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059713]").text(description); $(".js-view-count[data-work-id=36059713]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059713; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059713']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059713, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "52a4ff6a09f010d0a9710ac38f9db08d" } } $('.js-work-strip[data-work-id=36059713]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059713,"title":"Effects of soluble extracts from Leishmania infantum promastigotes, Toxoplasma gondii tachyzoites on TGF-b mediated pathways in activated CD4 þ T lymphocytes","translated_title":"","metadata":{"abstract":"Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. 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The interaction of the active cytokine with transforming growth factor-b receptor induces Foxp3 expression by activated lymphocytes, favoring their conversion through the T-regulatory phenotype. Both Toxoplasma gondii and L. infantum extracts are able to induce transforming growth factor-b production by activated T cells in the absence of accessory cells."},"translated_abstract":"Interference with transforming growth factor-b-mediated pathways helps several parasites to survive for long periods in immunocompetent hosts. Macrophages and dendritic cells infected by Toxoplasma, Leishmania and Plasmodium spp. produce large amounts of transforming growth factor-b and induce the differentiation of antigen-specific T-regulatory cells. Mechanisms not mediated by antigen-presentation could also account for the expansion of T-regulatory cells in parasitic diseases and they also might be mediated through transforming growth factor-b-receptor activated pathways. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059757"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059757/Stimulatory_Interactions_between_Human_Coronary_Smooth_Muscle_Cells_and_Dendritic_Cells"><img alt="Research paper thumbnail of Stimulatory Interactions between Human Coronary Smooth Muscle Cells and Dendritic Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/55945286/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059757/Stimulatory_Interactions_between_Human_Coronary_Smooth_Muscle_Cells_and_Dendritic_Cells">Stimulatory Interactions between Human Coronary Smooth Muscle Cells and Dendritic Cells</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Despite inflammatory and immune mechanisms participating to atherogenesis and dendritic cells (DC...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Despite inflammatory and immune mechanisms participating to atherogenesis and dendritic cells (DCs) driving immune and non-immune tissue injury response, the interactions between DCs and vascular smooth muscle cells (VSMCs) possibly relevant to vascular pathology including atherogenesis are still unclear. To address this issue, immature DCs (iDCs) generated from CD14 + cells isolated from healthy donors were matured either with cytokines (mDCs), or co-cultured (ccDCs) with human coronary artery VSMCs (CASMCs) using transwell chambers. Co-culture induced DC immunophenotypical and functional maturation similar to cytokines, as demonstrated by flow cytometry and mixed lymphocyte reaction. In turn, factors from mDCs and ccDCs induced CASMC migration. MCP-1 and TNFa, secreted from DCs, and IL-6 and MCP-1, secreted from CASMCs, were primarily involved. mDCs adhesion to CASMCs was enhanced by CASMC pre-treatment with IFNc and TNFa ICAM-1 and VCAM-1 were involved, since the expression of specific mRNAs for these molecules increased and adhesion was inhibited by neutralizing antibodies to the counter-receptors CD11c and CD18. Adhesion was also inhibited by CASMC pre-treatment with the HMG-CoA-reductase inhibitor atorvastatin and the PPARc agonist rosiglitazone, which suggests a further mechanism for the anti-inflammatory action of these drugs. Adhesion of DCs to VSMCs was shown also in vivo in rat carotid 7 to 21 days after crush and incision injury. The findings indicate that DCs and VSMCs can interact with reciprocal stimulation, possibly leading to perpetuate inflammation and vascular wall remodelling, and that the interaction is enhanced by a cytokine-rich inflammatory environment and down-regulated by HMGCoA-reductase inhibitors and PPARc agonists.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bdec44db94d2c0bc39101cad162891e7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945286,"asset_id":36059757,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945286/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059757"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059757"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059757; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059757]").text(description); $(".js-view-count[data-work-id=36059757]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059757; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059757']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059757, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bdec44db94d2c0bc39101cad162891e7" } } $('.js-work-strip[data-work-id=36059757]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059757,"title":"Stimulatory Interactions between Human Coronary Smooth Muscle Cells and Dendritic Cells","translated_title":"","metadata":{"abstract":"Despite inflammatory and immune mechanisms participating to atherogenesis and dendritic cells (DCs) driving immune and non-immune tissue injury response, the interactions between DCs and vascular smooth muscle cells (VSMCs) possibly relevant to vascular pathology including atherogenesis are still unclear. To address this issue, immature DCs (iDCs) generated from CD14 + cells isolated from healthy donors were matured either with cytokines (mDCs), or co-cultured (ccDCs) with human coronary artery VSMCs (CASMCs) using transwell chambers. Co-culture induced DC immunophenotypical and functional maturation similar to cytokines, as demonstrated by flow cytometry and mixed lymphocyte reaction. In turn, factors from mDCs and ccDCs induced CASMC migration. MCP-1 and TNFa, secreted from DCs, and IL-6 and MCP-1, secreted from CASMCs, were primarily involved. mDCs adhesion to CASMCs was enhanced by CASMC pre-treatment with IFNc and TNFa ICAM-1 and VCAM-1 were involved, since the expression of specific mRNAs for these molecules increased and adhesion was inhibited by neutralizing antibodies to the counter-receptors CD11c and CD18. Adhesion was also inhibited by CASMC pre-treatment with the HMG-CoA-reductase inhibitor atorvastatin and the PPARc agonist rosiglitazone, which suggests a further mechanism for the anti-inflammatory action of these drugs. Adhesion of DCs to VSMCs was shown also in vivo in rat carotid 7 to 21 days after crush and incision injury. The findings indicate that DCs and VSMCs can interact with reciprocal stimulation, possibly leading to perpetuate inflammation and vascular wall remodelling, and that the interaction is enhanced by a cytokine-rich inflammatory environment and down-regulated by HMGCoA-reductase inhibitors and PPARc agonists."},"translated_abstract":"Despite inflammatory and immune mechanisms participating to atherogenesis and dendritic cells (DCs) driving immune and non-immune tissue injury response, the interactions between DCs and vascular smooth muscle cells (VSMCs) possibly relevant to vascular pathology including atherogenesis are still unclear. To address this issue, immature DCs (iDCs) generated from CD14 + cells isolated from healthy donors were matured either with cytokines (mDCs), or co-cultured (ccDCs) with human coronary artery VSMCs (CASMCs) using transwell chambers. Co-culture induced DC immunophenotypical and functional maturation similar to cytokines, as demonstrated by flow cytometry and mixed lymphocyte reaction. In turn, factors from mDCs and ccDCs induced CASMC migration. MCP-1 and TNFa, secreted from DCs, and IL-6 and MCP-1, secreted from CASMCs, were primarily involved. mDCs adhesion to CASMCs was enhanced by CASMC pre-treatment with IFNc and TNFa ICAM-1 and VCAM-1 were involved, since the expression of specific mRNAs for these molecules increased and adhesion was inhibited by neutralizing antibodies to the counter-receptors CD11c and CD18. Adhesion was also inhibited by CASMC pre-treatment with the HMG-CoA-reductase inhibitor atorvastatin and the PPARc agonist rosiglitazone, which suggests a further mechanism for the anti-inflammatory action of these drugs. Adhesion of DCs to VSMCs was shown also in vivo in rat carotid 7 to 21 days after crush and incision injury. 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059766"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059766/Modulation_of_the_Immune_and_Inflammatory_Responses_by_Plasmodium_falciparum_Schizont_Extracts_Role_of_Myeloid_Dendritic_Cells_in_Effector_and_Regulatory_Functions_of_CD4_Lymphocytes"><img alt="Research paper thumbnail of Modulation of the Immune and Inflammatory Responses by Plasmodium falciparum Schizont Extracts: Role of Myeloid Dendritic Cells in Effector and Regulatory Functions of CD4 Lymphocytes" class="work-thumbnail" src="https://attachments.academia-assets.com/55945299/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059766/Modulation_of_the_Immune_and_Inflammatory_Responses_by_Plasmodium_falciparum_Schizont_Extracts_Role_of_Myeloid_Dendritic_Cells_in_Effector_and_Regulatory_Functions_of_CD4_Lymphocytes">Modulation of the Immune and Inflammatory Responses by Plasmodium falciparum Schizont Extracts: Role of Myeloid Dendritic Cells in Effector and Regulatory Functions of CD4 Lymphocytes</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The optimal immune response to malaria infection comprises rapid induction of inflammatory respon...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The optimal immune response to malaria infection comprises rapid induction of inflammatory responses promptly counteracted by regulatory mechanisms to prevent immunopathology. To evaluate the role of dendritic cells (DC) in the balance of parasite induced inflammatory/anti-inflammatory mechanisms, we studied the activity of monocyte-derived dendritic cells (MDDC), previously exposed to soluble extracts of Plasmodium falciparum-infected red blood cells (PfSE), in the differentiation of CD4 cells isolated from donors never exposed to malaria infection. We show that MDDC exposed to PfSE are extremely efficient to induce a contemporary differentiation of TH1 effector cells and T regulatory (Treg) cells in CD4 T cells even when exposed to low concentrations of parasitic extracts. Treg cells induced by MDDC infected with PfSE (MDDC-PfSE) produce transforming growth factor beta (TGF-) and interleukin 10 (IL-10) and are endowed with strong suppressive properties. They also show phenotypical and functional peculiarities, such as the contemporary expression of markers of Treg and TH1 differentiation and higher sensitivity to TLR4 ligands both inducing an increasing production of suppressive cytokines. On the whole, our data indicate that MDDC exposed to PfSE orchestrate a well-balanced immune response with timely differentiation of TH1 and Treg cells in CD4 cells from nonimmune donors and suggest that, during the infection, the role of MDCC could be particularly relevant in low-parasitemia conditions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="83064e5959971113151f489763a1176d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945299,"asset_id":36059766,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945299/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059766"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059766"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059766; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059766]").text(description); $(".js-view-count[data-work-id=36059766]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059766; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059766']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059766, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "83064e5959971113151f489763a1176d" } } $('.js-work-strip[data-work-id=36059766]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059766,"title":"Modulation of the Immune and Inflammatory Responses by Plasmodium falciparum Schizont Extracts: Role of Myeloid Dendritic Cells in Effector and Regulatory Functions of CD4 Lymphocytes","translated_title":"","metadata":{"abstract":"The optimal immune response to malaria infection comprises rapid induction of inflammatory responses promptly counteracted by regulatory mechanisms to prevent immunopathology. To evaluate the role of dendritic cells (DC) in the balance of parasite induced inflammatory/anti-inflammatory mechanisms, we studied the activity of monocyte-derived dendritic cells (MDDC), previously exposed to soluble extracts of Plasmodium falciparum-infected red blood cells (PfSE), in the differentiation of CD4 cells isolated from donors never exposed to malaria infection. We show that MDDC exposed to PfSE are extremely efficient to induce a contemporary differentiation of TH1 effector cells and T regulatory (Treg) cells in CD4 T cells even when exposed to low concentrations of parasitic extracts. Treg cells induced by MDDC infected with PfSE (MDDC-PfSE) produce transforming growth factor beta (TGF-) and interleukin 10 (IL-10) and are endowed with strong suppressive properties. 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059777"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059777/Haematological_parameters_natural_regulatory_CD4_CD25_FOXP3"><img alt="Research paper thumbnail of Haematological parameters natural regulatory CD4 CD25 FOXP3" class="work-thumbnail" src="https://attachments.academia-assets.com/55945312/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059777/Haematological_parameters_natural_regulatory_CD4_CD25_FOXP3">Haematological parameters natural regulatory CD4 CD25 FOXP3</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/MaritaTroyeblomberg">Marita Troye-blomberg</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Haematological parameters, natural regulatory CD4 + CD25 + FOXP3+ T cells and gδ T cells among tw...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Haematological parameters, natural regulatory CD4 + CD25 + FOXP3+ T cells and gδ T cells among two sympatric ethnic groups having different susceptibility to malaria in Burkina Faso Abstract Background: Fulani ethnic group individuals are less susceptible than sympatric Mossi ethnic group, in term of malaria infection severity, and differ in antibody production against malaria antigens. The differences in susceptibility to malaria between Fulani and Mossi ethnic groups are thought to be regulated by different genetic backgrounds and offer the opportunity to compare haematological parameters, Tregs and gδT cell profiles in seasonal and stable malaria transmission settings in Burkina Faso. The study was conducted at two different time points i.e. during the high and low malaria transmission period. Results: Two cross-sectional surveys were undertaken in adults above 20 years belonging either to the Fulani or the Mossi ethnic groups 1) at the peak of the malaria transmission season and 2) during the middle of the low malaria transmission season. Full blood counts, proportions of Tregs and gδ T cells were measured at both time-points. As previously shown the Fulani and Mossi ethnic groups showed a consistent difference in P. falciparum infection rates and parasite load. Differential white blood cell counts showed that the absolute lymphocyte counts were higher in the Mossi than in the Fulani ethnic group at both time points. While the proportion of CD4+CD25 high was higher in the Fulani ethnic group at the peak of malaria transmission season (p = 0.03), no clear pattern emerged for T regulatory cells expressing FoxP3 + and CD127 low. However CD3 + gδ + subpopulations were found to be higher in the Fulani compared to the Mossi ethnic group, and this difference was statistically significant at both time-points (p = 0.004 at low transmission season and p = 0.04 at peak of transmission). Conclusion: Our findings on regulatory T cell phenotypes suggest an interesting role for immune regulatory mechanisms in response to malaria. The study also suggests that TCRgδ + cells might contribute to the protection against malaria in the Fulani ethnic group involving their reported parasite inhibitory activities.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="4c3bf9a215cf1cbbe3f50eb258000323" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945312,"asset_id":36059777,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945312/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059777"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059777"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059777; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059777]").text(description); $(".js-view-count[data-work-id=36059777]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059777; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059777']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059777, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "4c3bf9a215cf1cbbe3f50eb258000323" } } $('.js-work-strip[data-work-id=36059777]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059777,"title":"Haematological parameters natural regulatory CD4 CD25 FOXP3","translated_title":"","metadata":{"abstract":"Haematological parameters, natural regulatory CD4 + CD25 + FOXP3+ T cells and gδ T cells among two sympatric ethnic groups having different susceptibility to malaria in Burkina Faso Abstract Background: Fulani ethnic group individuals are less susceptible than sympatric Mossi ethnic group, in term of malaria infection severity, and differ in antibody production against malaria antigens. The differences in susceptibility to malaria between Fulani and Mossi ethnic groups are thought to be regulated by different genetic backgrounds and offer the opportunity to compare haematological parameters, Tregs and gδT cell profiles in seasonal and stable malaria transmission settings in Burkina Faso. The study was conducted at two different time points i.e. during the high and low malaria transmission period. Results: Two cross-sectional surveys were undertaken in adults above 20 years belonging either to the Fulani or the Mossi ethnic groups 1) at the peak of the malaria transmission season and 2) during the middle of the low malaria transmission season. Full blood counts, proportions of Tregs and gδ T cells were measured at both time-points. As previously shown the Fulani and Mossi ethnic groups showed a consistent difference in P. falciparum infection rates and parasite load. Differential white blood cell counts showed that the absolute lymphocyte counts were higher in the Mossi than in the Fulani ethnic group at both time points. While the proportion of CD4+CD25 high was higher in the Fulani ethnic group at the peak of malaria transmission season (p = 0.03), no clear pattern emerged for T regulatory cells expressing FoxP3 + and CD127 low. However CD3 + gδ + subpopulations were found to be higher in the Fulani compared to the Mossi ethnic group, and this difference was statistically significant at both time-points (p = 0.004 at low transmission season and p = 0.04 at peak of transmission). Conclusion: Our findings on regulatory T cell phenotypes suggest an interesting role for immune regulatory mechanisms in response to malaria. The study also suggests that TCRgδ + cells might contribute to the protection against malaria in the Fulani ethnic group involving their reported parasite inhibitory activities."},"translated_abstract":"Haematological parameters, natural regulatory CD4 + CD25 + FOXP3+ T cells and gδ T cells among two sympatric ethnic groups having different susceptibility to malaria in Burkina Faso Abstract Background: Fulani ethnic group individuals are less susceptible than sympatric Mossi ethnic group, in term of malaria infection severity, and differ in antibody production against malaria antigens. The differences in susceptibility to malaria between Fulani and Mossi ethnic groups are thought to be regulated by different genetic backgrounds and offer the opportunity to compare haematological parameters, Tregs and gδT cell profiles in seasonal and stable malaria transmission settings in Burkina Faso. The study was conducted at two different time points i.e. during the high and low malaria transmission period. Results: Two cross-sectional surveys were undertaken in adults above 20 years belonging either to the Fulani or the Mossi ethnic groups 1) at the peak of the malaria transmission season and 2) during the middle of the low malaria transmission season. Full blood counts, proportions of Tregs and gδ T cells were measured at both time-points. As previously shown the Fulani and Mossi ethnic groups showed a consistent difference in P. falciparum infection rates and parasite load. Differential white blood cell counts showed that the absolute lymphocyte counts were higher in the Mossi than in the Fulani ethnic group at both time points. While the proportion of CD4+CD25 high was higher in the Fulani ethnic group at the peak of malaria transmission season (p = 0.03), no clear pattern emerged for T regulatory cells expressing FoxP3 + and CD127 low. However CD3 + gδ + subpopulations were found to be higher in the Fulani compared to the Mossi ethnic group, and this difference was statistically significant at both time-points (p = 0.004 at low transmission season and p = 0.04 at peak of transmission). Conclusion: Our findings on regulatory T cell phenotypes suggest an interesting role for immune regulatory mechanisms in response to malaria. The study also suggests that TCRgδ + cells might contribute to the protection against malaria in the Fulani ethnic group involving their reported parasite inhibitory activities.","internal_url":"https://www.academia.edu/36059777/Haematological_parameters_natural_regulatory_CD4_CD25_FOXP3","translated_internal_url":"","created_at":"2018-03-02T06:03:20.747-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136645,"work_id":36059777,"tagging_user_id":32025990,"tagged_user_id":null,"co_author_invite_id":6640229,"email":"e***o@ssss.gouv.qc.ca","display_order":1,"name":"E. 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36090518"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36090518/Interferon_a_and_Interleukin_2_Synergistically_Enhance_Basic_Fibroblast_Growth_Factor_Synthesis_and_Induce_Release_Promoting_Endothelial_Cell_Growth"><img alt="Research paper thumbnail of Interferon-a and Interleukin 2 Synergistically Enhance Basic Fibroblast Growth Factor Synthesis and Induce Release, Promoting Endothelial Cell Growth" class="work-thumbnail" src="https://attachments.academia-assets.com/55980090/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36090518/Interferon_a_and_Interleukin_2_Synergistically_Enhance_Basic_Fibroblast_Growth_Factor_Synthesis_and_Induce_Release_Promoting_Endothelial_Cell_Growth">Interferon-a and Interleukin 2 Synergistically Enhance Basic Fibroblast Growth Factor Synthesis and Induce Release, Promoting Endothelial Cell Growth</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">To elucidate mechanisms underlying neovascularization that accompanies certain chronic immune/ in...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">To elucidate mechanisms underlying neovascularization that accompanies certain chronic immune/ inflammatory disorders, the effects of interferon-a (IFN-a) and interleukin 2 (IL-2) on endothelial cell (EC) growth in vitro and angiogenesis in vivo were studied. Preincubation of cultured human ECs with IFN-a, followed by exposure to IL-2, resulted in effective stimulation of cell growth, whereas either cytokine alone had only a slight effect. The combination of IFN-a/IL-2 induced an an-giogenic response in the rabbit cornea. IL-2 receptor expression was enhanced on IFN-a-treated ECs: p55 was increased and p70 was induced. '25I-IL-2 binding to ECs treated with IFN-a was enhanced (Kd from 7 nM to 260 pM with IFN-a), and anti-p55 IgG blocked '25I-IL-2/EC interaction as well as IL-2-mediated EC proliferation. Consistent with these findings in cell culture, immunohistologic studies demonstrated p55 and p70 antigen in the vasculature of rheumatoid joints, but not in normal joint tissue. Exposure of cultured ECs to IFN-a increased levels of intracellular EC basic fibroblast growth factor (bFGF), and subsequent addition of IL-2 led to bFGF release into the medium. The observation that anti-bFGF IgG largely blocked EC proliferation in response to IFN-a/IL-2 suggested that bFGF was a critical agent in this setting. These data suggest a mechanism rendering ECs responsive to IL-2 which may be relevant in immune/inflammatory disorders: IFN-a-mediated induction of functional EC receptors for IL-2, which drives cell proliferation by a mechanism dependent on increased synthesis and release of bFGF. (J. Clin. Invest. 1993. 91:2504-2512.)</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="f0e6c1a7dfbbc49d1906727956ee4a78" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55980090,"asset_id":36090518,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55980090/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36090518"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36090518"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36090518; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36090518]").text(description); $(".js-view-count[data-work-id=36090518]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36090518; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36090518']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36090518, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "f0e6c1a7dfbbc49d1906727956ee4a78" } } $('.js-work-strip[data-work-id=36090518]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36090518,"title":"Interferon-a and Interleukin 2 Synergistically Enhance Basic Fibroblast Growth Factor Synthesis and Induce Release, Promoting Endothelial Cell Growth","translated_title":"","metadata":{"abstract":"To elucidate mechanisms underlying neovascularization that accompanies certain chronic immune/ inflammatory disorders, the effects of interferon-a (IFN-a) and interleukin 2 (IL-2) on endothelial cell (EC) growth in vitro and angiogenesis in vivo were studied. Preincubation of cultured human ECs with IFN-a, followed by exposure to IL-2, resulted in effective stimulation of cell growth, whereas either cytokine alone had only a slight effect. The combination of IFN-a/IL-2 induced an an-giogenic response in the rabbit cornea. IL-2 receptor expression was enhanced on IFN-a-treated ECs: p55 was increased and p70 was induced. '25I-IL-2 binding to ECs treated with IFN-a was enhanced (Kd from 7 nM to 260 pM with IFN-a), and anti-p55 IgG blocked '25I-IL-2/EC interaction as well as IL-2-mediated EC proliferation. Consistent with these findings in cell culture, immunohistologic studies demonstrated p55 and p70 antigen in the vasculature of rheumatoid joints, but not in normal joint tissue. Exposure of cultured ECs to IFN-a increased levels of intracellular EC basic fibroblast growth factor (bFGF), and subsequent addition of IL-2 led to bFGF release into the medium. The observation that anti-bFGF IgG largely blocked EC proliferation in response to IFN-a/IL-2 suggested that bFGF was a critical agent in this setting. These data suggest a mechanism rendering ECs responsive to IL-2 which may be relevant in immune/inflammatory disorders: IFN-a-mediated induction of functional EC receptors for IL-2, which drives cell proliferation by a mechanism dependent on increased synthesis and release of bFGF. (J. Clin. Invest. 1993. 91:2504-2512.)"},"translated_abstract":"To elucidate mechanisms underlying neovascularization that accompanies certain chronic immune/ inflammatory disorders, the effects of interferon-a (IFN-a) and interleukin 2 (IL-2) on endothelial cell (EC) growth in vitro and angiogenesis in vivo were studied. Preincubation of cultured human ECs with IFN-a, followed by exposure to IL-2, resulted in effective stimulation of cell growth, whereas either cytokine alone had only a slight effect. The combination of IFN-a/IL-2 induced an an-giogenic response in the rabbit cornea. IL-2 receptor expression was enhanced on IFN-a-treated ECs: p55 was increased and p70 was induced. '25I-IL-2 binding to ECs treated with IFN-a was enhanced (Kd from 7 nM to 260 pM with IFN-a), and anti-p55 IgG blocked '25I-IL-2/EC interaction as well as IL-2-mediated EC proliferation. Consistent with these findings in cell culture, immunohistologic studies demonstrated p55 and p70 antigen in the vasculature of rheumatoid joints, but not in normal joint tissue. Exposure of cultured ECs to IFN-a increased levels of intracellular EC basic fibroblast growth factor (bFGF), and subsequent addition of IL-2 led to bFGF release into the medium. The observation that anti-bFGF IgG largely blocked EC proliferation in response to IFN-a/IL-2 suggested that bFGF was a critical agent in this setting. These data suggest a mechanism rendering ECs responsive to IL-2 which may be relevant in immune/inflammatory disorders: IFN-a-mediated induction of functional EC receptors for IL-2, which drives cell proliferation by a mechanism dependent on increased synthesis and release of bFGF. (J. Clin. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059786"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059786/Sex_Differences_in_the_Response_to_Viral_Infections_TLR8_and_TLR9_Ligand_Stimulation_Induce_Higher_IL10_Production_in_Males"><img alt="Research paper thumbnail of Sex Differences in the Response to Viral Infections: TLR8 and TLR9 Ligand Stimulation Induce Higher IL10 Production in Males" class="work-thumbnail" src="https://attachments.academia-assets.com/55945323/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059786/Sex_Differences_in_the_Response_to_Viral_Infections_TLR8_and_TLR9_Ligand_Stimulation_Induce_Higher_IL10_Production_in_Males">Sex Differences in the Response to Viral Infections: TLR8 and TLR9 Ligand Stimulation Induce Higher IL10 Production in Males</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/LiviaCivitelli">Livia Civitelli</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Background: Susceptibility to viral infections as well as their severity are higher in men than i...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Background: Susceptibility to viral infections as well as their severity are higher in men than in women. Heightened antiviral responses typical of women are effective for rapid virus clearance, but if excessively high or prolonged, can result in chronic/ inflammatory pathologies. We investigated whether this variability could be in part attributable to differences in the response to the Toll-Like Receptors (TLR) more involved in the virus recognition.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="93a164ac713ea36782f898793c0d5f39" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945323,"asset_id":36059786,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945323/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059786"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059786"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059786; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059786]").text(description); $(".js-view-count[data-work-id=36059786]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059786; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059786']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059786, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "93a164ac713ea36782f898793c0d5f39" } } $('.js-work-strip[data-work-id=36059786]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059786,"title":"Sex Differences in the Response to Viral Infections: TLR8 and TLR9 Ligand Stimulation Induce Higher IL10 Production in Males","translated_title":"","metadata":{"abstract":"Background: Susceptibility to viral infections as well as their severity are higher in men than in women. 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wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059803/Low_molecular_weight_non_peptidic_agonists_of_TrkA_receptor_with_NGF_mimetic_activity">Low molecular weight, non-peptidic agonists of TrkA receptor with NGF-mimetic activity</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Exploitation of the biologic activity of neurotrophins is desirable for medical purposes, but the...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Exploitation of the biologic activity of neurotrophins is desirable for medical purposes, but their protein nature intrinsically bears adverse pharmacokinetic properties. Here, we report synthesis and biologic characterization of a novel class of low molecular weight, non-peptidic compounds with NGF (nerve growth factor)-mimetic properties. MT2, a representative compound, bound to Trk (tropomyosin kinase receptor)A chain on NGF-sensitive cells, as well as in cell-free assays, at nanomolar concentrations and induced TrkA autophosphorylation and receptor-mediated internalization. MT2 binding involved at least two amino-acid residues within TrkA molecule. Like NGF, MT2 increased phosphorylation of extracellular signal-regulated kinase1/2 and Akt proteins and production of MKP-1 phosphatase (dual specificity phosphatase 1), modulated p38 mitogen-activated protein kinase activation, sustained survival of serum-starved PC12 or RDG cells, and promoted their differentiation. However, the intensity of such responses was heterogenous, as the ability of maintaining survival was equally possessed by NGF and MT2, whereas the induction of differentiation was expressed at definitely lower levels by the mimetic. Analysis of TrkA autophosphorylation patterns induced by MT2 revealed a strong tyrosine (Tyr)490 and a limited Tyr785 and Tyr674/675 activation, findings coherent with the observed functional divarication. Consistently, in an NGF-deprived rat hippocampal neuronal model of Alzheimer Disease, MT2 could correct the biochemical abnormalities and sustain cell survival. Thus, NGF mimetics may reveal interesting investigational tools in neurobiology, as well as promising drug candidates.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="0a9b634c9553da9cdeb12c5e129ddedb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945341,"asset_id":36059803,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945341/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059803"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059803"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059803; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059803]").text(description); $(".js-view-count[data-work-id=36059803]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059803; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059803']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059803, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "0a9b634c9553da9cdeb12c5e129ddedb" } } $('.js-work-strip[data-work-id=36059803]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059803,"title":"Low molecular weight, non-peptidic agonists of TrkA receptor with NGF-mimetic activity","translated_title":"","metadata":{"abstract":"Exploitation of the biologic activity of neurotrophins is desirable for medical purposes, but their protein nature intrinsically bears adverse pharmacokinetic properties. 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However, the intensity of such responses was heterogenous, as the ability of maintaining survival was equally possessed by NGF and MT2, whereas the induction of differentiation was expressed at definitely lower levels by the mimetic. Analysis of TrkA autophosphorylation patterns induced by MT2 revealed a strong tyrosine (Tyr)490 and a limited Tyr785 and Tyr674/675 activation, findings coherent with the observed functional divarication. Consistently, in an NGF-deprived rat hippocampal neuronal model of Alzheimer Disease, MT2 could correct the biochemical abnormalities and sustain cell survival. Thus, NGF mimetics may reveal interesting investigational tools in neurobiology, as well as promising drug candidates."},"translated_abstract":"Exploitation of the biologic activity of neurotrophins is desirable for medical purposes, but their protein nature intrinsically bears adverse pharmacokinetic properties. 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However, the intensity of such responses was heterogenous, as the ability of maintaining survival was equally possessed by NGF and MT2, whereas the induction of differentiation was expressed at definitely lower levels by the mimetic. Analysis of TrkA autophosphorylation patterns induced by MT2 revealed a strong tyrosine (Tyr)490 and a limited Tyr785 and Tyr674/675 activation, findings coherent with the observed functional divarication. Consistently, in an NGF-deprived rat hippocampal neuronal model of Alzheimer Disease, MT2 could correct the biochemical abnormalities and sustain cell survival. 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mimetic","url":"https://www.academia.edu/Documents/in/NGF_mimetic"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36059824"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36059824/Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive_function_of_polyclonal_T_regulatory_cells_through_activation_of_TGFb_mediated_signals"><img alt="Research paper thumbnail of Plasmodium falciparum soluble extracts potentiate the suppressive function of polyclonal T regulatory cells through activation of TGFb-mediated signals" class="work-thumbnail" src="https://attachments.academia-assets.com/55945361/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36059824/Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive_function_of_polyclonal_T_regulatory_cells_through_activation_of_TGFb_mediated_signals">Plasmodium falciparum soluble extracts potentiate the suppressive function of polyclonal T regulatory cells through activation of TGFb-mediated signals</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AnnmariaClemente">Annmaria Clemente</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Increased numbers of T regulatory cells (Tregs), key mediators of immune homeostasis, were report...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Increased numbers of T regulatory cells (Tregs), key mediators of immune homeostasis, were reported in human and murine malaria and it is current opinion that these cells play a role in balancing protective immunity and pathogenesis during infection. However, the mechanisms governing their expansion during malaria infection are not completely defined. In this article we show that soluble extracts of Plasmodium falciparum (PfSEs), but not equivalent preparation of uninfected eryth-rocytes, induce the differentiation of polyclonally activated CD4 + cells in Tregs endowed with strong suppressive activity. PfSEs activate latent TGFb bound on the membrane of Treg cells, thus allowing the cytokine interaction with TGFb receptor, and inducing Foxp3 gene expression and TGFb production. The activation of membrane-bound latent TGFb by PfSEs is significantly reduced by a broad-spectrum metalloproteinases inhibitor with Zn ++-chelating activity, and completely inhibited by the combined action of such inhibitor and antibodies to a P. falciparum thrombospondin-related adhesive protein (PfTRAP). We conclude that Pf-Zn ++-dependent proteinases and, to a lesser extent, PfTRAP molecules are involved in the activation of latent TGFb bound on the membrane of activated Treg cells and suggest that, in malaria infection, this mechanism could contribute to the expansion of Tregs with different antigen specificity.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="81a150507b60446d9360e49702abfa4c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945361,"asset_id":36059824,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945361/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36059824"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36059824"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36059824; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36059824]").text(description); $(".js-view-count[data-work-id=36059824]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36059824; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36059824']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36059824, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "81a150507b60446d9360e49702abfa4c" } } $('.js-work-strip[data-work-id=36059824]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36059824,"title":"Plasmodium falciparum soluble extracts potentiate the suppressive function of polyclonal T regulatory cells through activation of TGFb-mediated signals","translated_title":"","metadata":{"abstract":"Increased numbers of T regulatory cells (Tregs), key mediators of immune homeostasis, were reported in human and murine malaria and it is current opinion that these cells play a role in balancing protective immunity and pathogenesis during infection. However, the mechanisms governing their expansion during malaria infection are not completely defined. In this article we show that soluble extracts of Plasmodium falciparum (PfSEs), but not equivalent preparation of uninfected eryth-rocytes, induce the differentiation of polyclonally activated CD4 + cells in Tregs endowed with strong suppressive activity. PfSEs activate latent TGFb bound on the membrane of Treg cells, thus allowing the cytokine interaction with TGFb receptor, and inducing Foxp3 gene expression and TGFb production. The activation of membrane-bound latent TGFb by PfSEs is significantly reduced by a broad-spectrum metalloproteinases inhibitor with Zn ++-chelating activity, and completely inhibited by the combined action of such inhibitor and antibodies to a P. falciparum thrombospondin-related adhesive protein (PfTRAP). We conclude that Pf-Zn ++-dependent proteinases and, to a lesser extent, PfTRAP molecules are involved in the activation of latent TGFb bound on the membrane of activated Treg cells and suggest that, in malaria infection, this mechanism could contribute to the expansion of Tregs with different antigen specificity."},"translated_abstract":"Increased numbers of T regulatory cells (Tregs), key mediators of immune homeostasis, were reported in human and murine malaria and it is current opinion that these cells play a role in balancing protective immunity and pathogenesis during infection. However, the mechanisms governing their expansion during malaria infection are not completely defined. In this article we show that soluble extracts of Plasmodium falciparum (PfSEs), but not equivalent preparation of uninfected eryth-rocytes, induce the differentiation of polyclonally activated CD4 + cells in Tregs endowed with strong suppressive activity. PfSEs activate latent TGFb bound on the membrane of Treg cells, thus allowing the cytokine interaction with TGFb receptor, and inducing Foxp3 gene expression and TGFb production. The activation of membrane-bound latent TGFb by PfSEs is significantly reduced by a broad-spectrum metalloproteinases inhibitor with Zn ++-chelating activity, and completely inhibited by the combined action of such inhibitor and antibodies to a P. falciparum thrombospondin-related adhesive protein (PfTRAP). We conclude that Pf-Zn ++-dependent proteinases and, to a lesser extent, PfTRAP molecules are involved in the activation of latent TGFb bound on the membrane of activated Treg cells and suggest that, in malaria infection, this mechanism could contribute to the expansion of Tregs with different antigen specificity.","internal_url":"https://www.academia.edu/36059824/Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive_function_of_polyclonal_T_regulatory_cells_through_activation_of_TGFb_mediated_signals","translated_internal_url":"","created_at":"2018-03-02T06:09:29.681-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31136695,"work_id":36059824,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Plasmodium falciparum soluble extracts potentiate the suppressive function of polyclonal T regulatory cells through activation of TGFb-mediated signals"},{"id":31136696,"work_id":36059824,"tagging_user_id":32025990,"tagged_user_id":32097049,"co_author_invite_id":null,"email":"a***e@virgilio.it","display_order":2,"name":"Annmaria Clemente","title":"Plasmodium falciparum soluble extracts potentiate the suppressive function of polyclonal T regulatory cells through activation of TGFb-mediated signals"}],"downloadable_attachments":[{"id":55945361,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945361/thumbnails/1.jpg","file_name":"Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive.pdf","download_url":"https://www.academia.edu/attachments/55945361/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Plasmodium_falciparum_soluble_extracts_p.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945361/Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive-libre.pdf?1519999979=\u0026response-content-disposition=attachment%3B+filename%3DPlasmodium_falciparum_soluble_extracts_p.pdf\u0026Expires=1732404749\u0026Signature=etySaAlh7XU4FUF6aIz87wLF7bPWyXffrGsRrc4duBcJyALP6jR8oCACpyzUSmUWC6sSGKvH51Xvk0XVYYA8yFhBWkzDY17xSorKoX1QUveFZiR9aXcwgpQ7SO6yoWTGyOXYy24nEEV~qTHxNhrjCKU3bu6UQHhNFN6Xvi56OoxIXTrSMFIKE-Hse~hdCQAWWPMUqKEFp3psTJ-BBGYGhhIMllwenNmQWmZYfCZaZVNJHr0BbmTi66k-u~6v55ZmQGdSntjYRfB7Yrjc~CTNfj9a52I44uVy-w3N6cj5IRf5W2ipz79ltTO1Si3Kdu3-Pb0ltdtnzpzKZBMBH46qVg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive_function_of_polyclonal_T_regulatory_cells_through_activation_of_TGFb_mediated_signals","translated_slug":"","page_count":11,"language":"en","content_type":"Work","owner":{"id":32025990,"first_name":"Maria Gabriella","middle_initials":"","last_name":"Torcia","page_name":"MariaGabriellaTorcia","domain_name":"unifi","created_at":"2015-06-09T07:13:10.551-07:00","display_name":"Maria Gabriella Torcia","url":"https://unifi.academia.edu/MariaGabriellaTorcia"},"attachments":[{"id":55945361,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/55945361/thumbnails/1.jpg","file_name":"Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive.pdf","download_url":"https://www.academia.edu/attachments/55945361/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE0OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Plasmodium_falciparum_soluble_extracts_p.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/55945361/Plasmodium_falciparum_soluble_extracts_potentiate_the_suppressive-libre.pdf?1519999979=\u0026response-content-disposition=attachment%3B+filename%3DPlasmodium_falciparum_soluble_extracts_p.pdf\u0026Expires=1732404749\u0026Signature=etySaAlh7XU4FUF6aIz87wLF7bPWyXffrGsRrc4duBcJyALP6jR8oCACpyzUSmUWC6sSGKvH51Xvk0XVYYA8yFhBWkzDY17xSorKoX1QUveFZiR9aXcwgpQ7SO6yoWTGyOXYy24nEEV~qTHxNhrjCKU3bu6UQHhNFN6Xvi56OoxIXTrSMFIKE-Hse~hdCQAWWPMUqKEFp3psTJ-BBGYGhhIMllwenNmQWmZYfCZaZVNJHr0BbmTi66k-u~6v55ZmQGdSntjYRfB7Yrjc~CTNfj9a52I44uVy-w3N6cj5IRf5W2ipz79ltTO1Si3Kdu3-Pb0ltdtnzpzKZBMBH46qVg__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":7823,"name":"Malaria","url":"https://www.academia.edu/Documents/in/Malaria"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060162"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060162/Hypoxia_mediated_induction_of_acidic_basic_fibroblast_growth_factor_and_platelet_derived_growth_factor_in_mononuclear_phagocytes_stimulates_growth_of_hypoxic_endothelial_cells_endothelium_angiogenesis"><img alt="Research paper thumbnail of Hypoxia-mediated induction of acidic/basic fibroblast growth factor and platelet-derived growth factor in mononuclear phagocytes stimulates growth of hypoxic endothelial cells (endothelium/angiogenesis" class="work-thumbnail" src="https://attachments.academia-assets.com/55945762/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060162/Hypoxia_mediated_induction_of_acidic_basic_fibroblast_growth_factor_and_platelet_derived_growth_factor_in_mononuclear_phagocytes_stimulates_growth_of_hypoxic_endothelial_cells_endothelium_angiogenesis">Hypoxia-mediated induction of acidic/basic fibroblast growth factor and platelet-derived growth factor in mononuclear phagocytes stimulates growth of hypoxic endothelial cells (endothelium/angiogenesis</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Wound repair and tumor vascularization depend upon blood vessel growth into hypoxic tissue. Altho...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Wound repair and tumor vascularization depend upon blood vessel growth into hypoxic tissue. Although hypoxia slows endothelial cell (EC) proliferation and suppresses EC basic fibroblast growth factor (bFGF) expression , we report that macrophages (MPs) exposed to Po2 12-14 torr (1 torr = 1333 Pa) synthesize and release in a time-dependent manner platelet-derived growth factor (PDGF) and acidic/basic FGFs (a/bFGFs), which stimulate the growth of hypoxic ECs. Chromatography of hypoxic MP-conditioned medium on immobilized heparin with an ascending NaCl gradient resolved three peaks of mitogenic activity: activity of the first peak was neutralized by antibody to PDGF; activity of the second peak was neutralized by antibody to aFGF; and activity of the third peak was neutralized by antibody to bFGF. Metabolically labeled lysates and supernatants from MPs exposed to hypoxia showed increased synthesis and release of immunoprecipitable PDGF and a/bFGF in the absence of changes in cell viability. Possible involvement of a heme-containing oxygen sensor in MP elaboration of growth factors was suggested by the induction of bFGF and PDGF by normoxic MPs exposed to nickel or cobalt, although metabolic inhibitors such as sodium azide were without effect. These results suggest a paracrine model in which hypoxia stimulates MP release of PDGF and a/bFGF, inducing EC proliferation and potentially promoting angiogenesis in hypoxic environments.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="8e7f7882c66714f0cde9ff6136db144c" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945762,"asset_id":36060162,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945762/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060162"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060162"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060162; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060162]").text(description); $(".js-view-count[data-work-id=36060162]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060162; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060162']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060162, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "8e7f7882c66714f0cde9ff6136db144c" } } $('.js-work-strip[data-work-id=36060162]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060162,"title":"Hypoxia-mediated induction of acidic/basic fibroblast growth factor and platelet-derived growth factor in mononuclear phagocytes stimulates growth of hypoxic endothelial cells (endothelium/angiogenesis","translated_title":"","metadata":{"abstract":"Wound repair and tumor vascularization depend upon blood vessel growth into hypoxic tissue. Although hypoxia slows endothelial cell (EC) proliferation and suppresses EC basic fibroblast growth factor (bFGF) expression , we report that macrophages (MPs) exposed to Po2 12-14 torr (1 torr = 1333 Pa) synthesize and release in a time-dependent manner platelet-derived growth factor (PDGF) and acidic/basic FGFs (a/bFGFs), which stimulate the growth of hypoxic ECs. Chromatography of hypoxic MP-conditioned medium on immobilized heparin with an ascending NaCl gradient resolved three peaks of mitogenic activity: activity of the first peak was neutralized by antibody to PDGF; activity of the second peak was neutralized by antibody to aFGF; and activity of the third peak was neutralized by antibody to bFGF. Metabolically labeled lysates and supernatants from MPs exposed to hypoxia showed increased synthesis and release of immunoprecipitable PDGF and a/bFGF in the absence of changes in cell viability. Possible involvement of a heme-containing oxygen sensor in MP elaboration of growth factors was suggested by the induction of bFGF and PDGF by normoxic MPs exposed to nickel or cobalt, although metabolic inhibitors such as sodium azide were without effect. These results suggest a paracrine model in which hypoxia stimulates MP release of PDGF and a/bFGF, inducing EC proliferation and potentially promoting angiogenesis in hypoxic environments."},"translated_abstract":"Wound repair and tumor vascularization depend upon blood vessel growth into hypoxic tissue. Although hypoxia slows endothelial cell (EC) proliferation and suppresses EC basic fibroblast growth factor (bFGF) expression , we report that macrophages (MPs) exposed to Po2 12-14 torr (1 torr = 1333 Pa) synthesize and release in a time-dependent manner platelet-derived growth factor (PDGF) and acidic/basic FGFs (a/bFGFs), which stimulate the growth of hypoxic ECs. Chromatography of hypoxic MP-conditioned medium on immobilized heparin with an ascending NaCl gradient resolved three peaks of mitogenic activity: activity of the first peak was neutralized by antibody to PDGF; activity of the second peak was neutralized by antibody to aFGF; and activity of the third peak was neutralized by antibody to bFGF. Metabolically labeled lysates and supernatants from MPs exposed to hypoxia showed increased synthesis and release of immunoprecipitable PDGF and a/bFGF in the absence of changes in cell viability. Possible involvement of a heme-containing oxygen sensor in MP elaboration of growth factors was suggested by the induction of bFGF and PDGF by normoxic MPs exposed to nickel or cobalt, although metabolic inhibitors such as sodium azide were without effect. These results suggest a paracrine model in which hypoxia stimulates MP release of PDGF and a/bFGF, inducing EC proliferation and potentially promoting angiogenesis in hypoxic environments.","internal_url":"https://www.academia.edu/36060162/Hypoxia_mediated_induction_of_acidic_basic_fibroblast_growth_factor_and_platelet_derived_growth_factor_in_mononuclear_phagocytes_stimulates_growth_of_hypoxic_endothelial_cells_endothelium_angiogenesis","translated_internal_url":"","created_at":"2018-03-02T06:55:17.476-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":32025990,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":31137006,"work_id":36060162,"tagging_user_id":32025990,"tagged_user_id":32024011,"co_author_invite_id":null,"email":"f***o@unifi.it","display_order":1,"name":"Federico Cozzolino","title":"Hypoxia-mediated induction of acidic/basic fibroblast growth factor and platelet-derived growth factor in mononuclear 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060143"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060143/Interferon_Induced_Inhibition_of_B16_Melanoma_Cell_Proliferation_Interference_with_the_bFGF_Autocrine_Growth_Circuit"><img alt="Research paper thumbnail of Interferon--Induced Inhibition of B16 Melanoma Cell Proliferation: Interference with the bFGF Autocrine Growth Circuit" class="work-thumbnail" src="https://attachments.academia-assets.com/55945737/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060143/Interferon_Induced_Inhibition_of_B16_Melanoma_Cell_Proliferation_Interference_with_the_bFGF_Autocrine_Growth_Circuit">Interferon--Induced Inhibition of B16 Melanoma Cell Proliferation: Interference with the bFGF Autocrine Growth Circuit</a></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The molecular mechanisms underlying the growth inhibition induced by interferon-(IFN-) in B16 mu-...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The molecular mechanisms underlying the growth inhibition induced by interferon-(IFN-) in B16 mu-rine melanoma cells were investigated. IFN-did not induce cell apoptosis, but strongly interfered with the synthesis of basic fibroblast growth factor (bFGF), which acts as an autocrine growth factor in this system. Inhibition of bFGF synthesis was observed at the same concentrations (50 –500 pM, 10 –100 U/ml) of IFN-able to induce growth arrest of B16 melanoma cells. Although the synthesis of acidic (a)FGF was only slightly affected by IFN-, the cytokine induced release of an aFGF-related low-molecular-weight pep-tide, which was able to interfere with bFGF binding to surface receptors. Thus, the molecular mechanisms of IFN-activity on melanoma cells include a specific modulation of the bFGF autocrine circuit.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bb88f68292eed20e8a501a632535d2dd" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945737,"asset_id":36060143,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945737/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060143"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060143"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060143; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060143]").text(description); $(".js-view-count[data-work-id=36060143]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060143; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060143']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060143, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bb88f68292eed20e8a501a632535d2dd" } } $('.js-work-strip[data-work-id=36060143]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060143,"title":"Interferon--Induced Inhibition of B16 Melanoma Cell Proliferation: Interference with the bFGF Autocrine Growth Circuit","translated_title":"","metadata":{"abstract":"The molecular mechanisms underlying the growth inhibition induced by interferon-(IFN-) in B16 mu-rine melanoma cells were investigated. 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IFN-did not induce cell apoptosis, but strongly interfered with the synthesis of basic fibroblast growth factor (bFGF), which acts as an autocrine growth factor in this system. Inhibition of bFGF synthesis was observed at the same concentrations (50 –500 pM, 10 –100 U/ml) of IFN-able to induce growth arrest of B16 melanoma cells. Although the synthesis of acidic (a)FGF was only slightly affected by IFN-, the cytokine induced release of an aFGF-related low-molecular-weight pep-tide, which was able to interfere with bFGF binding to surface receptors. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060130"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060130/NGF_Withdrawal_Induces_Apoptosis_in_CESS_B_Cell_Line_through_p38_MAPK_Activation_and_Bcl_2_Phosphorylation"><img alt="Research paper thumbnail of NGF Withdrawal Induces Apoptosis in CESS B Cell Line through p38 MAPK Activation and Bcl-2 Phosphorylation" class="work-thumbnail" src="https://attachments.academia-assets.com/55945726/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060130/NGF_Withdrawal_Induces_Apoptosis_in_CESS_B_Cell_Line_through_p38_MAPK_Activation_and_Bcl_2_Phosphorylation">NGF Withdrawal Induces Apoptosis in CESS B Cell Line through p38 MAPK Activation and Bcl-2 Phosphorylation</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/MariaLucibello">Maria Lucibello</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The sIgG lymphoblastoid B cell line CESS spontaneously produces a high amount of NGF and expresse...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The sIgG lymphoblastoid B cell line CESS spontaneously produces a high amount of NGF and expresses both high affinity (p140 Trk-A) and low affinity (p75 NTR) NGF receptors. Blocking NGF signals with neutralizing antibodies or specific Trk-A inhibitors induces a rapid phosphorylation of antiapoptotic Bcl-2 protein, followed by caspase activation, and apoptotic death of CESS cells. Bcl-2 phosphorylation in several sites within a 60 aa " loop " domain of protein is known to regulate its antiapoptotic function. Accordingly, CESS cells expressing the loop deletional mutant cDNA constructs Bcl-2 40-91 were completely resistant to apop-tosis induced by NGF withdrawal, indicating that Bcl-2 phosphorylation is a critical event. NGF withdrawal induces p38 MAPK, but not JNK, activation in CESS cells, and SB203580, a specific inhibitor of p38 MAPK, is able to prevent both Bcl-2 phosphorylation and apoptosis, indicating that p38 MAPK is the enzyme responsible for these events.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="ccd884fbe68aa70742539bc9207e9723" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945726,"asset_id":36060130,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945726/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060130"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060130"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060130; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060130]").text(description); $(".js-view-count[data-work-id=36060130]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060130; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060130']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060130, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "ccd884fbe68aa70742539bc9207e9723" } } $('.js-work-strip[data-work-id=36060130]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060130,"title":"NGF Withdrawal Induces Apoptosis in CESS B Cell Line through p38 MAPK Activation and Bcl-2 Phosphorylation","translated_title":"","metadata":{"abstract":"The sIgG lymphoblastoid B cell line CESS spontaneously produces a high amount of NGF and expresses both high affinity (p140 Trk-A) and low affinity (p75 NTR) NGF receptors. Blocking NGF signals with neutralizing antibodies or specific Trk-A inhibitors induces a rapid phosphorylation of antiapoptotic Bcl-2 protein, followed by caspase activation, and apoptotic death of CESS cells. Bcl-2 phosphorylation in several sites within a 60 aa \" loop \" domain of protein is known to regulate its antiapoptotic function. Accordingly, CESS cells expressing the loop deletional mutant cDNA constructs Bcl-2 40-91 were completely resistant to apop-tosis induced by NGF withdrawal, indicating that Bcl-2 phosphorylation is a critical event. NGF withdrawal induces p38 MAPK, but not JNK, activation in CESS cells, and SB203580, a specific inhibitor of p38 MAPK, is able to prevent both Bcl-2 phosphorylation and apoptosis, indicating that p38 MAPK is the enzyme responsible for these events."},"translated_abstract":"The sIgG lymphoblastoid B cell line CESS spontaneously produces a high amount of NGF and expresses both high affinity (p140 Trk-A) and low affinity (p75 NTR) NGF receptors. Blocking NGF signals with neutralizing antibodies or specific Trk-A inhibitors induces a rapid phosphorylation of antiapoptotic Bcl-2 protein, followed by caspase activation, and apoptotic death of CESS cells. Bcl-2 phosphorylation in several sites within a 60 aa \" loop \" domain of protein is known to regulate its antiapoptotic function. Accordingly, CESS cells expressing the loop deletional mutant cDNA constructs Bcl-2 40-91 were completely resistant to apop-tosis induced by NGF withdrawal, indicating that Bcl-2 phosphorylation is a critical event. 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="36060116"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/36060116/Nerve_Growth_Factor_Inhibits_Apoptosis_in_Memory_B_Lymphocytes_via_Inactivation_of_p38_MAPK_Prevention_of_Bcl_2_Phosphorylation_and_Cytochrome_c_Release"><img alt="Research paper thumbnail of Nerve Growth Factor Inhibits Apoptosis in Memory B Lymphocytes via Inactivation of p38 MAPK, Prevention of Bcl-2 Phosphorylation, and Cytochrome c Release" class="work-thumbnail" src="https://attachments.academia-assets.com/55945704/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/36060116/Nerve_Growth_Factor_Inhibits_Apoptosis_in_Memory_B_Lymphocytes_via_Inactivation_of_p38_MAPK_Prevention_of_Bcl_2_Phosphorylation_and_Cytochrome_c_Release">Nerve Growth Factor Inhibits Apoptosis in Memory B Lymphocytes via Inactivation of p38 MAPK, Prevention of Bcl-2 Phosphorylation, and Cytochrome c Release</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://unifi.academia.edu/MariaGabriellaTorcia">Maria Gabriella Torcia</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/SerenaAmmendola">Serena Ammendola</a></span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Survival of memory B lymphocytes is tightly linked to the integrity of the Bcl-2 protein and is r...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Survival of memory B lymphocytes is tightly linked to the integrity of the Bcl-2 protein and is regulated by a nerve growth factor (NGF) autocrine circuit. In factor-starved memory B cells, the addition of exogenous NGF promptly induced p38 mitogen-activated protein kinase (MAPK), but not c-Jun N-terminal kinase (JNK), dephos-phorylation. Conversely, withdrawal of endogenous NGF was followed by p38 MAPK activation and translo-cation onto mitochondria, whereby it combined with and phosphorylated Bcl-2, as assessed by co-immuno-precipitation and kinase assays in vivo and in vitro. Mitochondria isolated from human memory B cells, then exposed to recombinant p38 MAPK, released cyto-chrome c, as did mitochondria from Bcl-2-negative MDCK cells loaded with recombinant Bcl-2. Apoptosis induced by NGF neutralization could be blocked by the specific p38 MAPK inhibitor SB203580 or by Bcl-2 mutations in Ser-87 or Thr-56. These data demonstrate that the molecular mechanisms underlying the survival factor function of NGF critically rely upon the continuous inactivation of p38 MAPK, a Bcl-2-modifying enzyme.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7ccc9cbe64342332a85320bbda483667" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":55945704,"asset_id":36060116,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/55945704/download_file?st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&st=MTczMjQwMTE1MCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="36060116"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="36060116"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 36060116; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=36060116]").text(description); $(".js-view-count[data-work-id=36060116]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 36060116; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='36060116']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 36060116, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "7ccc9cbe64342332a85320bbda483667" } } $('.js-work-strip[data-work-id=36060116]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":36060116,"title":"Nerve Growth Factor Inhibits Apoptosis in Memory B Lymphocytes via Inactivation of p38 MAPK, Prevention of Bcl-2 Phosphorylation, and Cytochrome c Release","translated_title":"","metadata":{"abstract":"Survival of memory B lymphocytes is tightly linked to the integrity of the Bcl-2 protein and is regulated by a nerve growth factor (NGF) autocrine circuit. 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