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href="#Stomach"> <div class="vector-toc-text"> 3.1.1 Stomach </div> </a> <ul id="toc-Stomach-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Intestines" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Intestines"> <div class="vector-toc-text"> 3.1.2 Intestines </div> </a> <ul id="toc-Intestines-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Mycobiome" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Mycobiome"> <div class="vector-toc-text"> 3.2 Mycobiome </div> </a> <ul id="toc-Mycobiome-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Virome" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Virome"> <div class="vector-toc-text"> 3.3 Virome </div> </a> <ul id="toc-Virome-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Variation" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Variation"> <div class="vector-toc-text"> 4 Variation </div> </a> <button aria-controls="toc-Variation-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> Toggle Variation subsection </button> <ul id="toc-Variation-sublist" class="vector-toc-list"> <li id="toc-Age" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Age"> <div class="vector-toc-text"> 4.1 Age </div> </a> <ul id="toc-Age-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Geography" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Geography"> <div class="vector-toc-text"> 4.2 Geography </div> </a> <ul id="toc-Geography-sublist" class="vector-toc-list"> <li id="toc-Malnourishment" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Malnourishment"> <div class="vector-toc-text"> 4.2.1 Malnourishment </div> </a> <ul id="toc-Malnourishment-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Race_and_ethnicity" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Race_and_ethnicity"> <div class="vector-toc-text"> 4.3 Race and ethnicity </div> </a> <ul id="toc-Race_and_ethnicity-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Socioeconomic_status" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Socioeconomic_status"> <div class="vector-toc-text"> 4.4 Socioeconomic status </div> </a> <ul id="toc-Socioeconomic_status-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Antibiotic_Usage" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Antibiotic_Usage"> <div class="vector-toc-text"> 4.5 Antibiotic Usage </div> </a> <ul id="toc-Antibiotic_Usage-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Acquisition_in_human_infants" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Acquisition_in_human_infants"> <div class="vector-toc-text"> 5 Acquisition in human infants </div> </a> <ul id="toc-Acquisition_in_human_infants-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Functions" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Functions"> <div class="vector-toc-text"> 6 Functions </div> </a> <button aria-controls="toc-Functions-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> Toggle Functions subsection </button> <ul id="toc-Functions-sublist" class="vector-toc-list"> <li id="toc-Direct_inhibition_of_pathogens" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Direct_inhibition_of_pathogens"> <div class="vector-toc-text"> 6.1 Direct inhibition of pathogens </div> </a> <ul id="toc-Direct_inhibition_of_pathogens-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Development_of_enteric_protection_and_immune_system" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Development_of_enteric_protection_and_immune_system"> <div class="vector-toc-text"> 6.2 Development of enteric protection and immune system </div> </a> <ul id="toc-Development_of_enteric_protection_and_immune_system-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Metabolism" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Metabolism"> <div class="vector-toc-text"> 6.3 Metabolism </div> </a> <ul id="toc-Metabolism-sublist" class="vector-toc-list"> <li id="toc-Cellulose_degradation" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Cellulose_degradation"> <div class="vector-toc-text"> 6.3.1 Cellulose degradation </div> </a> <ul id="toc-Cellulose_degradation-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Pharmacomicrobiomics" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Pharmacomicrobiomics"> <div class="vector-toc-text"> 6.3.2 Pharmacomicrobiomics </div> </a> <ul id="toc-Pharmacomicrobiomics-sublist" class="vector-toc-list"> <li id="toc-Contribution_to_drug_metabolism" class="vector-toc-list-item vector-toc-level-4"> <a class="vector-toc-link" href="#Contribution_to_drug_metabolism"> <div class="vector-toc-text"> 6.3.2.1 Contribution to drug metabolism </div> </a> <ul id="toc-Contribution_to_drug_metabolism-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Secondary_metabolites" class="vector-toc-list-item vector-toc-level-4"> <a class="vector-toc-link" href="#Secondary_metabolites"> <div class="vector-toc-text"> 6.3.2.2 Secondary metabolites </div> </a> <ul id="toc-Secondary_metabolites-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Dysbiosis" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Dysbiosis"> <div class="vector-toc-text"> 6.3.3 Dysbiosis </div> </a> <ul id="toc-Dysbiosis-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Gut–brain_axis" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Gut–brain_axis"> <div class="vector-toc-text"> 6.4 Gut–brain axis </div> </a> <ul id="toc-Gut–brain_axis-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Alterations_in_microbiota_balance" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Alterations_in_microbiota_balance"> <div class="vector-toc-text"> 7 Alterations in microbiota balance </div> </a> <button aria-controls="toc-Alterations_in_microbiota_balance-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> Toggle Alterations in microbiota balance subsection </button> <ul id="toc-Alterations_in_microbiota_balance-sublist" class="vector-toc-list"> <li id="toc-Effects_of_antibiotic_use" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Effects_of_antibiotic_use"> <div class="vector-toc-text"> 7.1 Effects of antibiotic use </div> </a> <ul id="toc-Effects_of_antibiotic_use-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Pregnancy" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Pregnancy"> <div class="vector-toc-text"> 7.2 Pregnancy </div> </a> <ul id="toc-Pregnancy-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Probiotics,_prebiotics,_synbiotics,_and_pharmabiotics" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Probiotics,_prebiotics,_synbiotics,_and_pharmabiotics"> <div class="vector-toc-text"> 7.3 Probiotics, prebiotics, synbiotics, and pharmabiotics </div> </a> <ul id="toc-Probiotics,_prebiotics,_synbiotics,_and_pharmabiotics-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Fecal_floatation" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Fecal_floatation"> <div class="vector-toc-text"> 7.4 Fecal floatation </div> </a> <ul id="toc-Fecal_floatation-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Research" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Research"> <div class="vector-toc-text"> 7.5 Research </div> </a> <ul id="toc-Research-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Effects_of_exercise" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Effects_of_exercise"> <div class="vector-toc-text"> 7.6 Effects of exercise </div> </a> <ul id="toc-Effects_of_exercise-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Role_in_disease" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Role_in_disease"> <div class="vector-toc-text"> 8 Role in disease </div> </a> <button aria-controls="toc-Role_in_disease-sublist" class="cdx-button cdx-button--weight-quiet cdx-button--icon-only vector-toc-toggle"> Toggle Role in disease subsection </button> <ul id="toc-Role_in_disease-sublist" class="vector-toc-list"> <li id="toc-Ulcers" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Ulcers"> <div class="vector-toc-text"> 8.1 Ulcers </div> </a> <ul id="toc-Ulcers-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Bowel_perforation" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Bowel_perforation"> <div class="vector-toc-text"> 8.2 Bowel perforation </div> </a> <ul id="toc-Bowel_perforation-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Inflammatory_bowel_diseases" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Inflammatory_bowel_diseases"> <div class="vector-toc-text"> 8.3 Inflammatory bowel diseases </div> </a> <ul id="toc-Inflammatory_bowel_diseases-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Irritable_bowel_syndrome" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Irritable_bowel_syndrome"> <div class="vector-toc-text"> 8.4 Irritable bowel syndrome </div> </a> <ul id="toc-Irritable_bowel_syndrome-sublist" class="vector-toc-list"> <li id="toc-Asthma" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Asthma"> <div class="vector-toc-text"> 8.4.1 Asthma </div> </a> <ul id="toc-Asthma-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Diabetes_mellitus_type_1" class="vector-toc-list-item vector-toc-level-3"> <a class="vector-toc-link" href="#Diabetes_mellitus_type_1"> <div class="vector-toc-text"> 8.4.2 Diabetes mellitus type 1 </div> </a> <ul id="toc-Diabetes_mellitus_type_1-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Obesity_and_metabolic_syndrome" class="vector-toc-list-item vector-toc-level-2"> <a class="vector-toc-link" href="#Obesity_and_metabolic_syndrome"> <div class="vector-toc-text"> 8.5 Obesity and metabolic syndrome </div> </a> <ul id="toc-Obesity_and_metabolic_syndrome-sublist" class="vector-toc-list"> </ul> </li> </ul> </li> <li id="toc-Other_animals" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Other_animals"> <div class="vector-toc-text"> 9 Other animals </div> </a> <ul id="toc-Other_animals-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-See_also" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#See_also"> <div class="vector-toc-text"> 10 See also </div> </a> <ul id="toc-See_also-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Notes" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Notes"> <div class="vector-toc-text"> 11 Notes </div> </a> <ul id="toc-Notes-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-References" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#References"> <div class="vector-toc-text"> 12 References </div> </a> <ul id="toc-References-sublist" class="vector-toc-list"> </ul> </li> <li id="toc-Further_reading" class="vector-toc-list-item vector-toc-level-1"> <a class="vector-toc-link" href="#Further_reading"> <div class="vector-toc-text"> 13 Further reading </div> </a> <ul id="toc-Further_reading-sublist" class="vector-toc-list"> </ul> </li> </ul> </div> </div> </nav> </div> </div> <div class="mw-content-container"> <main id="content" class="mw-body"> <header class="mw-body-header vector-page-titlebar"> <nav aria-label="Contents" class="vector-toc-landmark"> <div id="vector-page-titlebar-toc" class="vector-dropdown vector-page-titlebar-toc vector-button-flush-left" > <input type="checkbox" id="vector-page-titlebar-toc-checkbox" role="button" aria-haspopup="true" data-event-name="ui.dropdown-vector-page-titlebar-toc" class="vector-dropdown-checkbox " aria-label="Toggle the table of contents" > <label id="vector-page-titlebar-toc-label" for="vector-page-titlebar-toc-checkbox" class="vector-dropdown-label cdx-button cdx-button--fake-button cdx-button--fake-button--enabled cdx-button--weight-quiet cdx-button--icon-only " aria-hidden="true" > Toggle the table of contents </label> <div class="vector-dropdown-content"> <div id="vector-page-titlebar-toc-unpinned-container" class="vector-unpinned-container"> </div> </div> </div> </nav> <h1 id="firstHeading" class="firstHeading mw-first-heading">Gut microbiota</h1> <div id="p-lang-btn" class="vector-dropdown mw-portlet mw-portlet-lang" > <input type="checkbox" id="p-lang-btn-checkbox" role="button" aria-haspopup="true" data-event-name="ui.dropdown-p-lang-btn" class="vector-dropdown-checkbox mw-interlanguage-selector" aria-label="Go to an article in another language. Available in 43 languages" > <label id="p-lang-btn-label" for="p-lang-btn-checkbox" class="vector-dropdown-label cdx-button cdx-button--fake-button cdx-button--fake-button--enabled cdx-button--weight-quiet cdx-button--action-progressive mw-portlet-lang-heading-43" aria-hidden="true" > 43 languages </label> <div class="vector-dropdown-content"> <div class="vector-menu-content"> <ul class="vector-menu-content-list"> <li class="interlanguage-link interwiki-ar mw-list-item"><a href="https://ar.wikipedia.org/wiki/%D9%86%D8%A8%D9%8A%D8%AA_%D8%AC%D8%B1%D8%AB%D9%88%D9%85%D9%8A_%D9%85%D8%B9%D9%88%D9%8A" title="نبيت جرثومي معوي – Arabic" lang="ar" hreflang="ar" data-title="نبيت جرثومي معوي" data-language-autonym="العربية" data-language-local-name="Arabic" class="interlanguage-link-target">العربية</a></li><li class="interlanguage-link interwiki-bn mw-list-item"><a href="https://bn.wikipedia.org/wiki/%E0%A6%86%E0%A6%A8%E0%A7%8D%E0%A6%A4%E0%A7%8D%E0%A6%B0%E0%A6%BF%E0%A6%95_%E0%A6%85%E0%A6%A3%E0%A7%81%E0%A6%9C%E0%A7%80%E0%A6%AC%E0%A6%B8%E0%A6%AE%E0%A6%97%E0%A7%8D%E0%A6%B0" title="আন্ত্রিক অণুজীবসমগ্র – Bangla" lang="bn" hreflang="bn" data-title="আন্ত্রিক অণুজীবসমগ্র" data-language-autonym="বাংলা" data-language-local-name="Bangla" class="interlanguage-link-target">বাংলা</a></li><li class="interlanguage-link interwiki-bg mw-list-item"><a href="https://bg.wikipedia.org/wiki/%D0%A7%D1%80%D0%B5%D0%B2%D0%BD%D0%B0_%D0%BC%D0%B8%D0%BA%D1%80%D0%BE%D1%84%D0%BB%D0%BE%D1%80%D0%B0" title="Чревна микрофлора – Bulgarian" lang="bg" hreflang="bg" data-title="Чревна микрофлора" data-language-autonym="Български" data-language-local-name="Bulgarian" class="interlanguage-link-target">Български</a></li><li class="interlanguage-link interwiki-bs mw-list-item"><a href="https://bs.wikipedia.org/wiki/Crijevna_mikrobiota" title="Crijevna mikrobiota – Bosnian" lang="bs" hreflang="bs" data-title="Crijevna mikrobiota" data-language-autonym="Bosanski" data-language-local-name="Bosnian" class="interlanguage-link-target">Bosanski</a></li><li class="interlanguage-link interwiki-ca mw-list-item"><a href="https://ca.wikipedia.org/wiki/Microbiota_intestinal" title="Microbiota intestinal – Catalan" lang="ca" hreflang="ca" data-title="Microbiota intestinal" data-language-autonym="Català" data-language-local-name="Catalan" class="interlanguage-link-target">Català</a></li><li class="interlanguage-link interwiki-cs mw-list-item"><a href="https://cs.wikipedia.org/wiki/St%C5%99evn%C3%AD_mikrofl%C3%B3ra" title="Střevní mikroflóra – Czech" lang="cs" hreflang="cs" data-title="Střevní mikroflóra" data-language-autonym="Čeština" data-language-local-name="Czech" class="interlanguage-link-target">Čeština</a></li><li class="interlanguage-link interwiki-da mw-list-item"><a href="https://da.wikipedia.org/wiki/Tarmflora" title="Tarmflora – Danish" lang="da" hreflang="da" data-title="Tarmflora" data-language-autonym="Dansk" data-language-local-name="Danish" class="interlanguage-link-target">Dansk</a></li><li class="interlanguage-link interwiki-de mw-list-item"><a href="https://de.wikipedia.org/wiki/Darmflora" title="Darmflora – German" lang="de" hreflang="de" data-title="Darmflora" data-language-autonym="Deutsch" data-language-local-name="German" class="interlanguage-link-target">Deutsch</a></li><li class="interlanguage-link interwiki-es mw-list-item"><a href="https://es.wikipedia.org/wiki/Microbiota_intestinal" title="Microbiota intestinal – Spanish" lang="es" hreflang="es" data-title="Microbiota intestinal" data-language-autonym="Español" data-language-local-name="Spanish" class="interlanguage-link-target">Español</a></li><li class="interlanguage-link interwiki-eo mw-list-item"><a href="https://eo.wikipedia.org/wiki/Intesta_mikrobioto" title="Intesta mikrobioto – Esperanto" lang="eo" hreflang="eo" data-title="Intesta mikrobioto" data-language-autonym="Esperanto" data-language-local-name="Esperanto" class="interlanguage-link-target">Esperanto</a></li><li class="interlanguage-link interwiki-eu mw-list-item"><a href="https://eu.wikipedia.org/wiki/Heste-flora" title="Heste-flora – Basque" lang="eu" hreflang="eu" data-title="Heste-flora" data-language-autonym="Euskara" data-language-local-name="Basque" class="interlanguage-link-target">Euskara</a></li><li class="interlanguage-link interwiki-fa mw-list-item"><a href="https://fa.wikipedia.org/wiki/%D9%81%D9%84%D9%88%D8%B1_%D9%85%DB%8C%DA%A9%D8%B1%D9%88%D8%A8%DB%8C_%D8%AF%D8%B3%D8%AA%DA%AF%D8%A7%D9%87_%DA%AF%D9%88%D8%A7%D8%B1%D8%B4" title="فلور میکروبی دستگاه گوارش – Persian" lang="fa" hreflang="fa" data-title="فلور میکروبی دستگاه گوارش" data-language-autonym="فارسی" data-language-local-name="Persian" class="interlanguage-link-target">فارسی</a></li><li class="interlanguage-link interwiki-fr mw-list-item"><a href="https://fr.wikipedia.org/wiki/Microbiote_intestinal_humain" title="Microbiote intestinal humain – French" lang="fr" hreflang="fr" data-title="Microbiote intestinal humain" data-language-autonym="Français" data-language-local-name="French" class="interlanguage-link-target">Français</a></li><li class="interlanguage-link interwiki-gl mw-list-item"><a href="https://gl.wikipedia.org/wiki/Flora_intestinal" title="Flora intestinal – Galician" lang="gl" hreflang="gl" data-title="Flora intestinal" data-language-autonym="Galego" data-language-local-name="Galician" class="interlanguage-link-target">Galego</a></li><li class="interlanguage-link interwiki-ko mw-list-item"><a href="https://ko.wikipedia.org/wiki/%EC%9E%A5%EB%82%B4%EB%AF%B8%EC%83%9D%EB%AC%BC%EA%B5%B0" title="장내미생물군 – Korean" lang="ko" hreflang="ko" data-title="장내미생물군" data-language-autonym="한국어" data-language-local-name="Korean" class="interlanguage-link-target">한국어</a></li><li class="interlanguage-link interwiki-hy mw-list-item"><a href="https://hy.wikipedia.org/wiki/%D4%B1%D5%B2%D5%AB%D6%84%D5%A1%D5%B5%D5%AB%D5%B6_%D6%86%D5%AC%D5%B8%D6%80%D5%A1" title="Աղիքային ֆլորա – Armenian" lang="hy" hreflang="hy" data-title="Աղիքային ֆլորա" data-language-autonym="Հայերեն" data-language-local-name="Armenian" class="interlanguage-link-target">Հայերեն</a></li><li class="interlanguage-link interwiki-hi mw-list-item"><a href="https://hi.wikipedia.org/wiki/%E0%A4%9C%E0%A4%A0%E0%A4%B0%E0%A4%BE%E0%A4%82%E0%A4%A4%E0%A5%8D%E0%A4%B0_%E0%A4%B5%E0%A4%A8%E0%A4%B8%E0%A5%8D%E0%A4%AA%E0%A4%A4%E0%A4%BF" title="जठरांत्र वनस्पति – Hindi" lang="hi" hreflang="hi" data-title="जठरांत्र वनस्पति" data-language-autonym="हिन्दी" data-language-local-name="Hindi" class="interlanguage-link-target">हिन्दी</a></li><li class="interlanguage-link interwiki-id mw-list-item"><a href="https://id.wikipedia.org/wiki/Mikrobiota_usus" title="Mikrobiota usus – Indonesian" lang="id" hreflang="id" data-title="Mikrobiota usus" 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data-title="Tarmflora" data-language-autonym="Norsk nynorsk" data-language-local-name="Norwegian Nynorsk" class="interlanguage-link-target">Norsk nynorsk</a></li><li class="interlanguage-link interwiki-uz mw-list-item"><a href="https://uz.wikipedia.org/wiki/Gut_microbiota" title="Gut microbiota – Uzbek" lang="uz" hreflang="uz" data-title="Gut microbiota" data-language-autonym="Oʻzbekcha / ўзбекча" data-language-local-name="Uzbek" class="interlanguage-link-target">Oʻzbekcha / ўзбекча</a></li><li class="interlanguage-link interwiki-pl mw-list-item"><a href="https://pl.wikipedia.org/wiki/Mikrobiota_jelitowa" title="Mikrobiota jelitowa – Polish" lang="pl" hreflang="pl" data-title="Mikrobiota jelitowa" data-language-autonym="Polski" data-language-local-name="Polish" class="interlanguage-link-target">Polski</a></li><li class="interlanguage-link interwiki-pt mw-list-item"><a href="https://pt.wikipedia.org/wiki/Microbiota_intestinal" title="Microbiota intestinal – Portuguese" lang="pt" hreflang="pt" data-title="Microbiota intestinal" data-language-autonym="Português" data-language-local-name="Portuguese" class="interlanguage-link-target">Português</a></li><li class="interlanguage-link interwiki-ro mw-list-item"><a href="https://ro.wikipedia.org/wiki/Flor%C4%83_intestinal%C4%83" title="Floră intestinală – Romanian" lang="ro" hreflang="ro" data-title="Floră intestinală" data-language-autonym="Română" data-language-local-name="Romanian" class="interlanguage-link-target">Română</a></li><li class="interlanguage-link interwiki-ru mw-list-item"><a href="https://ru.wikipedia.org/wiki/%D0%9C%D0%B8%D0%BA%D1%80%D0%BE%D1%84%D0%BB%D0%BE%D1%80%D0%B0_%D0%BA%D0%B8%D1%88%D0%B5%D1%87%D0%BD%D0%B8%D0%BA%D0%B0" title="Микрофлора кишечника – Russian" lang="ru" hreflang="ru" data-title="Микрофлора кишечника" data-language-autonym="Русский" data-language-local-name="Russian" class="interlanguage-link-target">Русский</a></li><li class="interlanguage-link interwiki-simple mw-list-item"><a href="https://simple.wikipedia.org/wiki/Gut_flora" title="Gut flora – Simple English" lang="en-simple" hreflang="en-simple" data-title="Gut flora" data-language-autonym="Simple English" data-language-local-name="Simple English" class="interlanguage-link-target">Simple English</a></li><li class="interlanguage-link interwiki-sl mw-list-item"><a href="https://sl.wikipedia.org/wiki/%C4%8Crevesna_flora" title="Črevesna flora – Slovenian" lang="sl" hreflang="sl" data-title="Črevesna flora" data-language-autonym="Slovenščina" data-language-local-name="Slovenian" class="interlanguage-link-target">Slovenščina</a></li><li class="interlanguage-link interwiki-sr mw-list-item"><a href="https://sr.wikipedia.org/wiki/Crevna_flora" title="Crevna flora – Serbian" lang="sr" hreflang="sr" data-title="Crevna flora" data-language-autonym="Српски / srpski" data-language-local-name="Serbian" class="interlanguage-link-target">Српски / srpski</a></li><li class="interlanguage-link interwiki-fi mw-list-item"><a href="https://fi.wikipedia.org/wiki/Normaalifloora" title="Normaalifloora – Finnish" lang="fi" hreflang="fi" data-title="Normaalifloora" data-language-autonym="Suomi" data-language-local-name="Finnish" class="interlanguage-link-target">Suomi</a></li><li class="interlanguage-link interwiki-sv mw-list-item"><a href="https://sv.wikipedia.org/wiki/Tarmflora" title="Tarmflora – Swedish" lang="sv" hreflang="sv" data-title="Tarmflora" data-language-autonym="Svenska" data-language-local-name="Swedish" class="interlanguage-link-target">Svenska</a></li><li class="interlanguage-link interwiki-tr mw-list-item"><a href="https://tr.wikipedia.org/wiki/Ba%C4%9F%C4%B1rsak_floras%C4%B1" title="Bağırsak florası – Turkish" lang="tr" hreflang="tr" data-title="Bağırsak florası" data-language-autonym="Türkçe" data-language-local-name="Turkish" class="interlanguage-link-target">Türkçe</a></li><li class="interlanguage-link interwiki-uk mw-list-item"><a href="https://uk.wikipedia.org/wiki/%D0%A4%D0%BB%D0%BE%D1%80%D0%B0_%D0%BA%D0%B8%D1%88%D0%BA%D0%B8" title="Флора кишки – Ukrainian" lang="uk" hreflang="uk" data-title="Флора кишки" data-language-autonym="Українська" data-language-local-name="Ukrainian" class="interlanguage-link-target">Українська</a></li><li class="interlanguage-link interwiki-vi mw-list-item"><a href="https://vi.wikipedia.org/wiki/H%E1%BB%87_vi_sinh_%C4%91%C6%B0%E1%BB%9Dng_ru%E1%BB%99t" title="Hệ vi sinh đường ruột – Vietnamese" lang="vi" hreflang="vi" data-title="Hệ vi sinh đường ruột" data-language-autonym="Tiếng Việt" data-language-local-name="Vietnamese" class="interlanguage-link-target">Tiếng Việt</a></li><li class="interlanguage-link interwiki-zh mw-list-item"><a href="https://zh.wikipedia.org/wiki/%E8%85%B8%E9%81%93%E8%8F%8C%E7%BE%A4" title="腸道菌群 – Chinese" lang="zh" hreflang="zh" data-title="腸道菌群" data-language-autonym="中文" data-language-local-name="Chinese" class="interlanguage-link-target">中文</a></li> </ul> 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i{font-style:normal}.mw-parser-output .hatnote+link+.hatnote{margin-top:-0.5em}@media print{body.ns-0 .mw-parser-output .hatnote{display:none!important}}</style><div role="note" class="hatnote navigation-not-searchable">"Enteric bacteria" redirects here. For other uses, see <a href="/wiki/Enteric_bacteria_(disambiguation)" class="mw-disambig" title="Enteric bacteria (disambiguation)">Enteric bacteria (disambiguation)</a>.</div> <figure class="mw-default-size mw-halign-right" typeof="mw:File/Thumb"><a href="/wiki/File:E._coli_Bacteria_(7316101966).jpg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/3/3a/E._coli_Bacteria_%287316101966%29.jpg/220px-E._coli_Bacteria_%287316101966%29.jpg" decoding="async" width="220" height="185" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/3/3a/E._coli_Bacteria_%287316101966%29.jpg/330px-E._coli_Bacteria_%287316101966%29.jpg 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/3/3a/E._coli_Bacteria_%287316101966%29.jpg/440px-E._coli_Bacteria_%287316101966%29.jpg 2x" data-file-width="2100" data-file-height="1766" /></a><figcaption><a href="/wiki/Escherichia_coli" title="Escherichia coli">Escherichia coli</a>, one of the many species of <a href="/wiki/Bacteria" title="Bacteria">bacteria</a> present in the human gut</figcaption></figure> Gut microbiota, gut microbiome, or gut flora are the <a href="/wiki/Microorganism" title="Microorganism">microorganisms</a>, including <a href="/wiki/Bacteria" title="Bacteria">bacteria</a>, <a href="/wiki/Archaea" title="Archaea">archaea</a>, <a href="/wiki/Fungi" class="mw-redirect" title="Fungi">fungi</a>, and <a href="/wiki/Viruses" class="mw-redirect" title="Viruses">viruses</a>, that live in the <a href="/wiki/Digestive_tracts" class="mw-redirect" title="Digestive tracts">digestive tracts</a> of <a href="/wiki/Animal" title="Animal">animals</a>.<a href="#cite_note-Moszak-1">[1]</a><a href="#cite_note-Engel-2">[2]</a> The gastrointestinal <a href="/wiki/Metagenome" class="mw-redirect" title="Metagenome">metagenome</a> is the aggregate of all the <a href="/wiki/Genome" title="Genome">genomes</a> of the gut <a href="/wiki/Microbiota" title="Microbiota">microbiota</a>.<a href="#cite_note-Segata-3">[3]</a><a href="#cite_note-Saxena2016-4">[4]</a> The <a href="/wiki/Gastrointestinal_tract" title="Gastrointestinal tract">gut</a> is the main location of the <a href="/wiki/Human_microbiome" title="Human microbiome">human microbiome</a>.<a href="#cite_note-Prescotts-5">[5]</a> The gut microbiota has broad impacts, including effects on <a href="/wiki/Colonisation_(biology)" title="Colonisation (biology)">colonization</a>, resistance to <a href="/wiki/Pathogen" title="Pathogen">pathogens</a>, maintaining the <a href="/wiki/Intestinal_epithelium" title="Intestinal epithelium">intestinal epithelium</a>, metabolizing dietary and pharmaceutical compounds, controlling immune function, and even behavior through the <a href="/wiki/Gut%E2%80%93brain_axis" title="Gut–brain axis">gut–brain axis</a>.<a href="#cite_note-Saxena2016-4">[4]</a> The microbial composition of the gut microbiota varies across regions of the digestive tract. The <a href="/wiki/Colon_(anatomy)" class="mw-redirect" title="Colon (anatomy)">colon</a> contains the highest microbial density of any human-associated microbial community studied so far, representing between 300 and 1000 different <a href="/wiki/Species" title="Species">species</a>.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a> Bacteria are the largest and to date, best studied component and 99% of gut bacteria come from about 30 or 40 species.<a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a> Up to 60% of the dry mass of <a href="/wiki/Feces" title="Feces">feces</a> is bacteria.<a href="#cite_note-Stephen_and_Cummings-8">[8]</a> Over 99% of the bacteria in the gut are <a href="/wiki/Anaerobe" class="mw-redirect" title="Anaerobe">anaerobes</a>, but in the <a href="/wiki/Cecum" title="Cecum">cecum</a>, <a href="/wiki/Aerobic_bacteria" class="mw-redirect" title="Aerobic bacteria">aerobic bacteria</a> reach high densities.<a href="#cite_note-Prescotts-5">[5]</a> It is estimated that the human gut microbiota have around a hundred times as many <a href="/wiki/Gene" title="Gene">genes</a> as there are in the <a href="/wiki/Human_genome" title="Human genome">human genome</a>. <meta property="mw:PageProp/toc" /> <div class="mw-heading mw-heading2"><h2 id="Overview">Overview</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=1" title="Edit section: Overview">edit</a>]</div> <figure typeof="mw:File/Thumb"><a href="/wiki/File:Composition_and_distribution_of_intestinal_microflora.jpg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/9/97/Composition_and_distribution_of_intestinal_microflora.jpg/300px-Composition_and_distribution_of_intestinal_microflora.jpg" decoding="async" width="300" height="298" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/9/97/Composition_and_distribution_of_intestinal_microflora.jpg/450px-Composition_and_distribution_of_intestinal_microflora.jpg 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/9/97/Composition_and_distribution_of_intestinal_microflora.jpg/600px-Composition_and_distribution_of_intestinal_microflora.jpg 2x" data-file-width="4030" data-file-height="4009" /></a><figcaption>Composition and distribution of gut microbiota in human body</figcaption></figure> In humans, the gut microbiota has the highest numbers and species of bacteria compared to other areas of the body.<a href="#cite_note-Quigley2013rev-9">[9]</a> The approximate number of bacteria composing the gut microbiota is about 1013–1014 (10,000 to 100,000 billion).<a href="#cite_note-10">[10]</a> In humans, the gut flora is established at birth and gradually transitions towards a state resembling that of adults by the age of two,<a href="#cite_note-11">[11]</a> coinciding with the development and maturation of the <a href="/wiki/Intestinal_epithelium" title="Intestinal epithelium">intestinal epithelium</a> and <a href="/wiki/Intestinal_mucosal_barrier" title="Intestinal mucosal barrier">intestinal mucosal barrier</a>. This barrier is essential for supporting a symbiotic relationship with the gut flora while providing protection against pathogenic organisms.<a href="#cite_note-Sommer2013rev-12">[12]</a><a href="#cite_note-Faderl2015rev-13">[13]</a> The relationship between some gut microbiota and humans is not merely <a href="/wiki/Commensalism" title="Commensalism">commensal</a> (a non-harmful coexistence), but rather a <a href="/wiki/Mutualism_(biology)" title="Mutualism (biology)">mutualistic</a> relationship.<a href="#cite_note-Prescotts-5">[5]</a>: 700  Some human gut microorganisms benefit the host by <a href="/wiki/Fermentation" title="Fermentation">fermenting</a> <a href="/wiki/Dietary_fiber" title="Dietary fiber">dietary fiber</a> into <a href="/wiki/Short-chain_fatty_acid" title="Short-chain fatty acid">short-chain fatty acids</a> (SCFAs), such as <a href="/wiki/Acetic_acid" title="Acetic acid">acetic acid</a> and <a href="/wiki/Butyric_acid" title="Butyric acid">butyric acid</a>, which are then absorbed by the host.<a href="#cite_note-Quigley2013rev-9">[9]</a><a href="#cite_note-Clarke2014rev-14">[14]</a> Intestinal <a href="/wiki/Bacteria" title="Bacteria">bacteria</a> also play a role in synthesizing certain <a href="/wiki/B_vitamins" title="B vitamins">B vitamins</a> and <a href="/wiki/Vitamin_K" title="Vitamin K">vitamin K</a> as well as metabolizing <a href="/wiki/Bile_acid" title="Bile acid">bile acids</a>, <a href="/wiki/Sterol" title="Sterol">sterols</a>, and <a href="/wiki/Xenobiotic" title="Xenobiotic">xenobiotics</a>.<a href="#cite_note-Prescotts-5">[5]</a><a href="#cite_note-Clarke2014rev-14">[14]</a> The systemic importance of the SCFAs and other compounds they produce are like <a href="/wiki/Hormones" class="mw-redirect" title="Hormones">hormones</a> and the gut flora itself appears to function like an <a href="/wiki/Gland" title="Gland">endocrine organ</a>.<a href="#cite_note-Clarke2014rev-14">[14]</a> Dysregulation of the gut flora has been correlated with a host of inflammatory and autoimmune conditions.<a href="#cite_note-Quigley2013rev-9">[9]</a><a href="#cite_note-Shen2016rev-15">[15]</a> The composition of human gut microbiota changes over time, when the diet changes, and as overall health changes.<a href="#cite_note-Quigley2013rev-9">[9]</a><a href="#cite_note-Shen2016rev-15">[15]</a> A <a href="/wiki/Systematic_review" title="Systematic review">systematic review</a> from 2016 examined the preclinical and small human trials that have been conducted with certain commercially available strains of probiotic bacteria and identified those that had the most potential to be useful for certain <a href="/wiki/Central_nervous_system_disorder" class="mw-redirect" title="Central nervous system disorder">central nervous system disorders</a>.<a href="#cite_note-CNS_SystRev_2016-16">[16]</a> It should also be highlighted that the Mediterranean diet, rich in vegetables and fibers, stimulates the activity and growth of beneficial bacteria for the brain.<a href="#cite_note-Microbiome_summary-17">[17]</a> <div class="mw-heading mw-heading2"><h2 id="Classifications">Classifications</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=2" title="Edit section: Classifications">edit</a>]</div> The microbial composition of the gut microbiota varies across the digestive tract. In the <a href="/wiki/Stomach" title="Stomach">stomach</a> and <a href="/wiki/Small_intestine" title="Small intestine">small intestine</a>, relatively few species of bacteria are generally present.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a><a href="#cite_note-Sears-18">[18]</a> The <a href="/wiki/Colon_(anatomy)" class="mw-redirect" title="Colon (anatomy)">colon</a>, in contrast, contains the highest microbial density of any human-associated microbial community studied so far<a href="#cite_note-19">[19]</a> with between 1010 and 1011 (10 to 100 billion) cells per gram of intestinal content.<a href="#cite_note-20">[20]</a> These bacteria represent between 300 and 1000 different <a href="/wiki/Species" title="Species">species</a>.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a><a href="#cite_note-Sears-18">[18]</a> However, 99% of the bacteria come from about 30 or 40 species.<a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a> As a consequence of their abundance in the intestine, bacteria also make up to 60% of the dry mass of <a href="/wiki/Feces" title="Feces">feces</a>.<a href="#cite_note-Stephen_and_Cummings-8">[8]</a> <a href="/wiki/Fungi" class="mw-redirect" title="Fungi">Fungi</a>, <a href="/wiki/Protist" title="Protist">protists</a>, <a href="/wiki/Archaea" title="Archaea">archaea</a>, and <a href="/wiki/Virus" title="Virus">viruses</a> are also present in the gut flora, but less is known about their activities.<a href="#cite_note-Lozupone2012-21">[21]</a> Over 99% of the bacteria in the gut are <a href="/wiki/Anaerobe" class="mw-redirect" title="Anaerobe">anaerobes</a>, but in the <a href="/wiki/Cecum" title="Cecum">cecum</a>, <a href="/wiki/Aerobic_bacteria" class="mw-redirect" title="Aerobic bacteria">aerobic bacteria</a> reach high densities.<a href="#cite_note-Prescotts-5">[5]</a> It is estimated that these gut flora have around a hundred times as many <a href="/wiki/Gene" title="Gene">genes</a> in total as there are in the <a href="/wiki/Human_genome" title="Human genome">human genome</a>.<a href="#cite_note-22">[22]</a> <figure class="mw-default-size" typeof="mw:File/Thumb"><a href="/wiki/File:Candida_albicans.jpg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/b/b6/Candida_albicans.jpg/220px-Candida_albicans.jpg" decoding="async" width="220" height="165" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/b/b6/Candida_albicans.jpg/330px-Candida_albicans.jpg 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/b/b6/Candida_albicans.jpg/440px-Candida_albicans.jpg 2x" data-file-width="640" data-file-height="480" /></a><figcaption><a href="/wiki/Candida_albicans" title="Candida albicans">Candida albicans</a>, a dimorphic fungus that grows as a yeast in the gut</figcaption></figure> Many species in the gut have not been studied outside of their hosts because they cannot be <a href="/wiki/Microbiological_culture" title="Microbiological culture">cultured</a>.<a href="#cite_note-Sears-18">[18]</a><a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a><a href="#cite_note-Shanahan-23">[23]</a> While there are a small number of core microbial species shared by most individuals, populations of microbes can vary widely.<a href="#cite_note-Tap-24">[24]</a> Within an individual, their microbial populations stay fairly constant over time, with some alterations occurring due to changes in lifestyle, diet and age.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a><a href="#cite_note-OHara06-25">[25]</a> The <a href="/wiki/Human_Microbiome_Project" title="Human Microbiome Project">Human Microbiome Project</a> has set out to better describe the <a href="/wiki/Microbiota" title="Microbiota">microbiota</a> of the human gut and other body locations.[<a href="/wiki/Wikipedia:Citation_needed" title="Wikipedia:Citation needed">citation needed</a>] The four dominant <a href="/wiki/Bacterial_phyla" title="Bacterial phyla">bacterial phyla</a> in the human gut are <a href="/wiki/Bacillota" title="Bacillota">Bacillota</a> (Firmicutes), <a href="/wiki/Bacteroidota" title="Bacteroidota">Bacteroidota</a>, <a href="/wiki/Actinomycetota" title="Actinomycetota">Actinomycetota</a>, and <a href="/wiki/Pseudomonadota" title="Pseudomonadota">Pseudomonadota</a>.<a href="#cite_note-pmid24388028-26">[26]</a> Most bacteria belong to the genera <a href="/wiki/Bacteroides" title="Bacteroides">Bacteroides</a>, <a href="/wiki/Clostridium" title="Clostridium">Clostridium</a>, <a href="/wiki/Faecalibacterium" title="Faecalibacterium">Faecalibacterium</a>,<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a><a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a> <a href="/wiki/Eubacterium" title="Eubacterium">Eubacterium</a>, <a href="/wiki/Ruminococcus" title="Ruminococcus">Ruminococcus</a>, <a href="/wiki/Peptococcus" title="Peptococcus">Peptococcus</a>, <a href="/wiki/Peptostreptococcus" title="Peptostreptococcus">Peptostreptococcus</a>, and <a href="/wiki/Bifidobacterium" title="Bifidobacterium">Bifidobacterium</a>.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a><a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a> Other genera, such as <a href="/wiki/Escherichia" title="Escherichia">Escherichia</a> and <a href="/wiki/Lactobacillus" title="Lactobacillus">Lactobacillus</a>, are present to a lesser extent.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a> Species from the genus Bacteroides alone constitute about 30% of all bacteria in the gut, suggesting that this genus is especially important in the functioning of the host.<a href="#cite_note-Sears-18">[18]</a> Fungal genera that have been detected in the gut include <a href="/wiki/Candida_(genus)" class="mw-redirect" title="Candida (genus)">Candida</a>, <a href="/wiki/Saccharomyces" title="Saccharomyces">Saccharomyces</a>, <a href="/wiki/Aspergillus" title="Aspergillus">Aspergillus</a>, <a href="/wiki/Penicillium" title="Penicillium">Penicillium</a>, <a href="/wiki/Rhodotorula" title="Rhodotorula">Rhodotorula</a>, <a href="/wiki/Trametes" title="Trametes">Trametes</a>, <a href="/wiki/Pleospora" title="Pleospora">Pleospora</a>, <a href="/wiki/Sclerotinia" title="Sclerotinia">Sclerotinia</a>, <a href="/wiki/Bullera" title="Bullera">Bullera</a>, and <a href="/wiki/Galactomyces" title="Galactomyces">Galactomyces</a>, among others.<a href="#cite_note-mycobiome-27">[27]</a><a href="#cite_note-SIFO-28">[28]</a> Rhodotorula is most frequently found in individuals with <a href="/wiki/Inflammatory_bowel_disease" title="Inflammatory bowel disease">inflammatory bowel disease</a> while Candida is most frequently found in individuals with hepatitis B cirrhosis and chronic hepatitis B.<a href="#cite_note-mycobiome-27">[27]</a> Due to the prevalence of fungi in the natural environment, determining which genera and species are permanent members of the gut <a href="/wiki/Mycobiome" title="Mycobiome">mycobiome</a> is difficult.<a href="#cite_note-29">[29]</a><a href="#cite_note-Quadram-30">[30]</a> Research is underway as to whether Penicillium is a permanent or transient member of the gut flora, obtained from dietary sources such as <a href="/wiki/Cheese" title="Cheese">cheese</a>, though several species in the genus are known to survive at temperatures around 37°C, around the same as the <a href="/wiki/Human_body_temperature" title="Human body temperature">core body temperature</a>.<a href="#cite_note-Quadram-30">[30]</a> <a href="/wiki/Saccharomyces_cerevisiae" title="Saccharomyces cerevisiae">Saccharomyces cerevisiae</a>, brewer's yeast, is known to reach the intestines after being ingested and can be responsible for the condition <a href="/wiki/Auto-brewery_syndrome" title="Auto-brewery syndrome">auto-brewery syndrome</a> in cases where it is overabundant,<a href="#cite_note-Quadram-30">[30]</a><a href="#cite_note-31">[31]</a><a href="#cite_note-32">[32]</a> while <a href="/wiki/Candida_albicans" title="Candida albicans">Candida albicans</a> is likely a permanent member, and is believed to be acquired at birth through <a href="/wiki/Vertical_transmission" title="Vertical transmission">vertical transmission</a>.<a href="#cite_note-33">[33]</a>[<a href="/wiki/Wikipedia:Identifying_reliable_sources_(medicine)" title="Wikipedia:Identifying reliable sources (medicine)">medical citation needed</a>] <a href="/wiki/Methanobrevibacter_smithii" title="Methanobrevibacter smithii">Archaea</a> constitute another large class of gut flora which are important in the metabolism of the bacterial products of fermentation. <a href="/wiki/Industrialisation" title="Industrialisation">Industrialization</a> is associated with changes in the microbiota and the reduction of diversity could drive certain species to extinction; in 2018, researchers proposed a <a href="/wiki/Biobank" title="Biobank">biobank</a> repository of human microbiota.<a href="#cite_note-34">[34]</a> <div class="mw-heading mw-heading3"><h3 id="Enterotype">Enterotype</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=3" title="Edit section: Enterotype">edit</a>]</div> An <a href="/wiki/Enterotype" title="Enterotype">enterotype</a> is a classification of living organisms based on its bacteriological <a href="/wiki/Ecosystem" title="Ecosystem">ecosystem</a> in the human gut microbiome not dictated by age, gender, body weight, or national divisions.<a href="#cite_note-Nature-35">[35]</a> There are indications that long-term diet influences enterotype.<a href="#cite_note-Wu_et_al-36">[36]</a> Three human enterotypes have been proposed,<a href="#cite_note-Nature-35">[35]</a><a href="#cite_note-37">[37]</a> but their value has been questioned.<a href="#cite_note-2014cellhostandmicrobentero-38">[38]</a> <div class="mw-heading mw-heading2"><h2 id="Composition">Composition</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=4" title="Edit section: Composition">edit</a>]</div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">See also: <a href="/wiki/Human_microbiome#Gastrointestinal_tract" title="Human microbiome">Human microbiome § Gastrointestinal tract</a></div> <div class="mw-heading mw-heading3"><h3 id="Bacteriome">Bacteriome</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=5" title="Edit section: Bacteriome">edit</a>]</div> <div class="mw-heading mw-heading4"><h4 id="Stomach">Stomach</h4>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=6" title="Edit section: Stomach">edit</a>]</div> Due to the high acidity of the <a href="/wiki/Stomach" title="Stomach">stomach</a>, most microorganisms cannot survive there. The main bacteria of the gastric microbiota belong to five major phyla: <a href="/wiki/Firmicutes" class="mw-redirect" title="Firmicutes">Firmicutes</a>, <a href="/wiki/Bacteroidetes" class="mw-redirect" title="Bacteroidetes">Bacteroidetes</a>, <a href="/wiki/Actinobacteria_(class)" class="mw-redirect" title="Actinobacteria (class)">Actinobacteria</a>, <a href="/wiki/Fusobacteriota" title="Fusobacteriota">Fusobacteriota</a>, and <a href="/wiki/Proteobacteria" class="mw-redirect" title="Proteobacteria">Proteobacteria</a>. The dominant genera are <a href="/wiki/Prevotella" title="Prevotella">Prevotella</a>, <a href="/wiki/Streptococcus" title="Streptococcus">Streptococcus</a>, <a href="/wiki/Veillonella" title="Veillonella">Veillonella</a>, <a href="/wiki/Rothia_(bacterium)" title="Rothia (bacterium)">Rothia </a>, and <a href="/wiki/Haemophilus" title="Haemophilus">Haemophilus</a>.<a href="#cite_note-Nardone-39">[39]</a> The interaction between the pre-existing gastric microbiota with the introduction of <a href="/wiki/H._pylori" class="mw-redirect" title="H. pylori">H. pylori</a> may influence <a href="/wiki/Helicobacter_pylori#Infection" title="Helicobacter pylori">disease progression</a>.<a href="#cite_note-Nardone-39">[39]</a> When there is a presence of H. pylori it becomes the dominant of the microbiota.<a href="#cite_note-Yao-40">[40]</a> <div class="mw-heading mw-heading4"><h4 id="Intestines">Intestines</h4>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=7" title="Edit section: Intestines">edit</a>]</div> <table class="wikitable" style="float: right; margin-left:15px; text-align:center"> <tbody><tr> <td colspan="2">Bacteria commonly found in the human colon<a href="#cite_note-TxtbookBacteriology-41">[41]</a> </td></tr> <tr> <th>Bacterium </th> <th>Incidence (%) </th></tr> <tr> <td><a href="/wiki/Bacteroides_fragilis" title="Bacteroides fragilis">Bacteroides fragilis</a> </td> <td style="text-align:right;">100 </td></tr> <tr> <td><a href="/wiki/Bacteroides_melaninogenicus" class="mw-redirect" title="Bacteroides melaninogenicus">Bacteroides melaninogenicus</a> </td> <td style="text-align:right;">100 </td></tr> <tr> <td><a href="/w/index.php?title=Bacteroides_oralis&action=edit&redlink=1" class="new" title="Bacteroides oralis (page does not exist)">Bacteroides oralis</a> </td> <td style="text-align:right;">100 </td></tr> <tr> <td><a href="/wiki/Enterococcus_faecalis" title="Enterococcus faecalis">Enterococcus faecalis</a> </td> <td style="text-align:right;">100 </td></tr> <tr> <td><a href="/wiki/Escherichia_coli" title="Escherichia coli">Escherichia coli</a> </td> <td style="text-align:right;">100 </td></tr> <tr> <td><a href="/wiki/Enterobacter" title="Enterobacter">Enterobacter</a> sp. </td> <td style="text-align:right;">40–80 </td></tr> <tr> <td><a href="/wiki/Klebsiella" title="Klebsiella">Klebsiella</a> sp. </td> <td style="text-align:right;">40–80 </td></tr> <tr> <td><a href="/wiki/Bifidobacterium_bifidum" title="Bifidobacterium bifidum">Bifidobacterium bifidum</a> </td> <td style="text-align:right;">30–70 </td></tr> <tr> <td><a href="/wiki/Staphylococcus_aureus" title="Staphylococcus aureus">Staphylococcus aureus</a> </td> <td style="text-align:right;">30–50 </td></tr> <tr> <td><a href="/wiki/Lactobacillus" title="Lactobacillus">Lactobacillus</a> </td> <td style="text-align:right;">20–60 </td></tr> <tr> <td><a href="/wiki/Clostridium_perfringens" title="Clostridium perfringens">Clostridium perfringens</a> </td> <td style="text-align:right;">25–35 </td></tr> <tr> <td><a href="/wiki/Proteus_mirabilis" title="Proteus mirabilis">Proteus mirabilis</a> </td> <td style="text-align:right;">5–55 </td></tr> <tr> <td><a href="/wiki/Clostridium_tetani" title="Clostridium tetani">Clostridium tetani</a> </td> <td style="text-align:right;">1–35 </td></tr> <tr> <td><a href="/wiki/Clostridium_septicum" title="Clostridium septicum">Clostridium septicum</a> </td> <td style="text-align:right;">5–25 </td></tr> <tr> <td><a href="/wiki/Pseudomonas_aeruginosa" title="Pseudomonas aeruginosa">Pseudomonas aeruginosa</a> </td> <td style="text-align:right;">3–11 </td></tr> <tr> <td><a href="/wiki/Salmonella_enterica" title="Salmonella enterica">Salmonella enterica</a> </td> <td style="text-align:right;">3–7 </td></tr> <tr> <td><a href="/wiki/Faecalibacterium_prausnitzii" class="mw-redirect" title="Faecalibacterium prausnitzii">Faecalibacterium prausnitzii</a> </td> <td style="text-align:right;">?common </td></tr> <tr> <td><a href="/wiki/Peptostreptococcus" title="Peptostreptococcus">Peptostreptococcus</a> sp. </td> <td style="text-align:right;">?common </td></tr> <tr> <td><a href="/wiki/Peptococcus" title="Peptococcus">Peptococcus</a> sp. </td> <td style="text-align:right;">?common </td></tr></tbody></table> The small intestine contains a trace amount of microorganisms due to the proximity and influence of the stomach. <a href="/wiki/Gram-positive_bacteria" title="Gram-positive bacteria">Gram-positive</a> <a href="/wiki/Coccus" class="mw-redirect" title="Coccus">cocci</a> and <a href="/wiki/Bacillus_(shape)" class="mw-redirect" title="Bacillus (shape)">rod-shaped bacteria</a> are the predominant microorganisms found in the small intestine.<a href="#cite_note-Prescotts-5">[5]</a> However, in the distal portion of the small intestine alkaline conditions support gram-negative bacteria of the Enterobacteriaceae.<a href="#cite_note-Prescotts-5">[5]</a> The bacterial flora of the small intestine aid in a wide range of intestinal functions. The bacterial flora provide regulatory signals that enable the development and utility of the gut. Overgrowth of bacteria in the small intestine can lead to intestinal failure.<a href="#cite_note-quigley2006-42">[42]</a> In addition the large intestine contains the largest bacterial ecosystem in the human body.<a href="#cite_note-Prescotts-5">[5]</a> About 99% of the large intestine and feces flora are made up of obligate anaerobes such as Bacteroides and Bifidobacterium.<a href="#cite_note-43">[43]</a> Factors that disrupt the microorganism population of the large intestine include antibiotics, stress, and parasites.<a href="#cite_note-Prescotts-5">[5]</a> Bacteria make up most of the flora in the <a href="/wiki/Colon_(anatomy)" class="mw-redirect" title="Colon (anatomy)">colon</a><a href="#cite_note-University_of_Glasgow-44">[44]</a> and accounts for 60% of <a href="/wiki/Fecal" class="mw-redirect" title="Fecal">fecal</a> nitrogen.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a> This fact makes feces an ideal source of gut flora for any tests and experiments by extracting the nucleic acid from fecal specimens, and bacterial 16S rRNA gene sequences are generated with bacterial primers. This form of testing is also often preferable to more invasive techniques, such as biopsies. Five <a href="/wiki/Phylum" title="Phylum">phyla</a> dominate the intestinal microbiota: <a href="/wiki/Bacteroidota" title="Bacteroidota">Bacteroidota</a>, <a href="/wiki/Bacillota" title="Bacillota">Bacillota</a> (Firmicutes), <a href="/wiki/Actinomycetota" title="Actinomycetota">Actinomycetota</a>, <a href="/wiki/Pseudomonadota" title="Pseudomonadota">Pseudomonadota</a>, and <a href="/wiki/Verrucomicrobiota" title="Verrucomicrobiota">Verrucomicrobiota</a> – with Bacteroidota and Bacillota constituting 90% of the composition.<a href="#cite_note-pmid26963713-45">[45]</a> Somewhere between 300<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a> and 1000 different <a href="/wiki/Species" title="Species">species</a> live in the gut,<a href="#cite_note-Sears-18">[18]</a> with most estimates at about 500.<a href="#cite_note-Steinhoff-46">[46]</a><a href="#cite_note-gibson-47">[47]</a> However, it is probable that 99% of the bacteria come from about 30 or 40 species, with <a href="/wiki/Faecalibacterium_prausnitzii" class="mw-redirect" title="Faecalibacterium prausnitzii">Faecalibacterium prausnitzii</a> (phylum firmicutes) being the most common species in healthy adults.<a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a><a href="#cite_note-48">[48]</a> Research suggests that the relationship between gut <a href="/wiki/Flora_(microbiology)" title="Flora (microbiology)">flora</a> and humans is not merely <a href="/wiki/Commensalism" title="Commensalism">commensal</a> (a non-harmful coexistence), but rather is a <a href="/wiki/Mutualism_(biology)" title="Mutualism (biology)">mutualistic</a>, <a href="/wiki/Symbiosis" title="Symbiosis">symbiotic</a> relationship.<a href="#cite_note-Sears-18">[18]</a> Though people can survive with no gut flora,<a href="#cite_note-Steinhoff-46">[46]</a> the microorganisms perform a host of useful functions, such as <a href="/wiki/Fermentation_(biochemistry)" class="mw-redirect" title="Fermentation (biochemistry)">fermenting</a> unused energy substrates, training the <a href="/wiki/Immune_system" title="Immune system">immune system</a> via end products of metabolism like <a href="/wiki/Propionate" class="mw-redirect" title="Propionate">propionate</a> and <a href="/wiki/Acetate" title="Acetate">acetate</a>, preventing growth of harmful species, regulating the development of the gut, producing vitamins for the host (such as <a href="/wiki/Biotin" title="Biotin">biotin</a> and <a href="/wiki/Vitamin_K" title="Vitamin K">vitamin K</a>), and producing hormones to direct the host to store fats.<a href="#cite_note-Prescotts-5">[5]</a> Extensive modification and imbalances of the gut microbiota and its microbiome or gene collection are associated with obesity.<a href="#cite_note-49">[49]</a> However, in certain conditions, some species are thought to be capable of causing <a href="/wiki/Disease" title="Disease">disease</a> by causing <a href="/wiki/Infection" title="Infection">infection</a> or increasing <a href="/wiki/Cancer" title="Cancer">cancer</a> risk for the host.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a><a href="#cite_note-University_of_Glasgow-44">[44]</a> <div class="mw-heading mw-heading3"><h3 id="Mycobiome">Mycobiome</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=8" title="Edit section: Mycobiome">edit</a>]</div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Further information: <a href="/wiki/Mycobiome" title="Mycobiome">Mycobiome</a></div> <a href="/wiki/Fungus" title="Fungus">Fungi</a> and <a href="/wiki/Protist" title="Protist">protists</a> also make up a part of the gut flora, but less is known about their activities.<a href="#cite_note-Nash_et_al_2017-50">[50]</a> <div class="mw-heading mw-heading3"><h3 id="Virome">Virome</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=9" title="Edit section: Virome">edit</a>]</div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Further information: <a href="/wiki/Virome" title="Virome">Virome</a></div> The <a href="/wiki/Human_virome" title="Human virome">human virome</a> is mostly <a href="/wiki/Bacteriophage" title="Bacteriophage">bacteriophages</a>.<a href="#cite_note-ScarpelliniIaniro2015-51">[51]</a> <div class="mw-heading mw-heading2"><h2 id="Variation">Variation</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=10" title="Edit section: Variation">edit</a>]</div> <div class="mw-heading mw-heading3"><h3 id="Age">Age</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=11" title="Edit section: Age">edit</a>]</div> There are common patterns of microbiome composition evolution during life.<a href="#cite_note-Gerritsen_et_al_2012-52">[52]</a> In general, the diversity of microbiota composition of fecal samples is significantly higher in adults than in children, although interpersonal differences are higher in children than in adults.<a href="#cite_note-Tanya_Yatsunenko_2012-53">[53]</a> Much of the maturation of microbiota into an adult-like configuration happens during the first three years of life.<a href="#cite_note-Tanya_Yatsunenko_2012-53">[53]</a> As the microbiome composition changes, so does the composition of bacterial proteins produced in the gut. In adult microbiomes, a high prevalence of enzymes involved in <a href="/wiki/Fermentation" title="Fermentation">fermentation</a>, <a href="/wiki/Methanogenesis" title="Methanogenesis">methanogenesis</a> and the metabolism of <a href="/wiki/Arginine" title="Arginine">arginine</a>, <a href="/wiki/Glutamate" class="mw-redirect" title="Glutamate">glutamate</a>, <a href="/wiki/Aspartate" class="mw-redirect" title="Aspartate">aspartate</a> and <a href="/wiki/Lysine" title="Lysine">lysine</a> have been found. In contrast, in infant microbiomes the dominant enzymes are involved in <a href="/wiki/Cysteine" title="Cysteine">cysteine</a> metabolism and fermentation pathways.<a href="#cite_note-Tanya_Yatsunenko_2012-53">[53]</a> <div class="mw-heading mw-heading3"><h3 id="Geography">Geography</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=12" title="Edit section: Geography">edit</a>]</div> Gut microbiome composition depends on the geographic origin of populations. Variations in a trade-off of <a href="/wiki/Prevotella" title="Prevotella">Prevotella</a>, the representation of the <a href="/wiki/Urease" title="Urease">urease</a> gene, and the representation of genes encoding glutamate synthase/degradation or other enzymes involved in amino acids degradation or vitamin biosynthesis show significant differences between populations from the US, <a href="/wiki/Malawi" title="Malawi">Malawi</a>, or Amerindian origin.<a href="#cite_note-Tanya_Yatsunenko_2012-53">[53]</a> The US population has a high representation of enzymes encoding the degradation of <a href="/wiki/Glutamine" title="Glutamine">glutamine</a> and enzymes involved in vitamin and <a href="/wiki/Lipoic_acid" title="Lipoic acid">lipoic acid</a> biosynthesis; whereas Malawi and Amerindian populations have a high representation of enzymes encoding glutamate synthase and they also have an overrepresentation of <a href="/wiki/%CE%91-amylase" class="mw-redirect" title="Α-amylase">α-amylase</a> in their microbiomes. As the US population has a diet richer in fats than Amerindian or Malawian populations which have a corn-rich diet, the diet is probably the main determinant of the gut bacterial composition.<a href="#cite_note-Tanya_Yatsunenko_2012-53">[53]</a> Further studies have indicated a large difference in the composition of microbiota between European and rural African children. The fecal bacteria of children from <a href="/wiki/Florence" title="Florence">Florence</a> were compared to that of children from the small rural village of <a href="/wiki/Boulpon" title="Boulpon">Boulpon</a> in <a href="/wiki/Burkina_Faso" title="Burkina Faso">Burkina Faso</a>. The diet of a typical child living in this village is largely lacking in fats and animal proteins and rich in polysaccharides and plant proteins. The fecal bacteria of European children were dominated by Firmicutes and showed a marked reduction in biodiversity, while the fecal bacteria of the Boulpon children was dominated by Bacteroidetes. The increased biodiversity and different composition of the gut microbiome in African populations may aid in the digestion of normally indigestible plant polysaccharides and also may result in a reduced incidence of non-infectious colonic diseases.<a href="#cite_note-Carlotta_De_Filippo_2010-54">[54]</a> On a smaller scale, it has been shown that sharing numerous common environmental exposures in a family is a strong determinant of individual microbiome composition. This effect has no genetic influence and it is consistently observed in culturally different populations.<a href="#cite_note-Tanya_Yatsunenko_2012-53">[53]</a> <div class="mw-heading mw-heading4"><h4 id="Malnourishment">Malnourishment</h4>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=13" title="Edit section: Malnourishment">edit</a>]</div> <a href="/wiki/Malnutrition" title="Malnutrition">Malnourished</a> children have less mature and less diverse gut microbiota than healthy children, and changes in the microbiome associated with nutrient scarcity can in turn be a pathophysiological cause of malnutrition.<a href="#cite_note-Jonkers-55">[55]</a><a href="#cite_note-Million-56">[56]</a> Malnourished children also typically have more potentially pathogenic gut flora, and more <a href="/wiki/Yeast" title="Yeast">yeast</a> in their mouths and throats.<a href="#cite_note-Rytter-57">[57]</a> Altering diet may lead to changes in gut microbiota composition and diversity.<a href="#cite_note-Alcocketal2014-58">[58]</a> <div class="mw-heading mw-heading3"><h3 id="Race_and_ethnicity">Race and ethnicity</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=14" title="Edit section: Race and ethnicity">edit</a>]</div> Researchers with the American Gut Project and Human Microbiome Project found that twelve microbe families varied in abundance based on the race or ethnicity of the individual. The strength of these associations is limited by the small sample size: the American Gut Project collected data from 1,375 individuals, 90% of whom were white.<a href="#cite_note-Renson-59">[59]</a> The Healthy Life in an Urban Setting (HELIUS) study in Amsterdam found that those of Dutch ancestry had the highest level of gut microbiota diversity, while those of South Asian and <a href="/wiki/Surinamese_people" title="Surinamese people">Surinamese</a> descent had the lowest diversity. The study results suggested that individuals of the same race or ethnicity have more similar microbiomes than individuals of different racial backgrounds.<a href="#cite_note-Renson-59">[59]</a> <div class="mw-heading mw-heading3"><h3 id="Socioeconomic_status">Socioeconomic status</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=15" title="Edit section: Socioeconomic status">edit</a>]</div> As of 2020, at least two studies have demonstrated a link between an individual's <a href="/wiki/Socioeconomic_status" title="Socioeconomic status">socioeconomic status</a> (SES) and their gut microbiota. A study in <a href="/wiki/Chicago" title="Chicago">Chicago</a> found that individuals in higher SES neighborhoods had greater microbiota diversity. People from higher SES neighborhoods also had more abundant Bacteroides bacteria. Similarly, a study of <a href="/wiki/Twin" title="Twin">twins</a> in the United Kingdom found that higher SES was also linked with a greater gut diversity.<a href="#cite_note-Renson-59">[59]</a> <div class="mw-heading mw-heading3"><h3 id="Antibiotic_Usage">Antibiotic Usage</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=16" title="Edit section: Antibiotic Usage">edit</a>]</div> As of 2023, a study suggests that antibiotics, especially those used in the treatment of broad-spectrum bacterial infections, have negative effects on the gut microbiota.<a href="#cite_note-60">[60]</a> The study also states that there are many experts on intestinal health concerned that antibody usage has reduced the diversity of the gut microbiota, many of the strains are lost, and if there is a re-emergence of the bacteria, is gradual and long-term. <a href="#cite_note-61">[61]</a> <div class="mw-heading mw-heading2"><h2 id="Acquisition_in_human_infants">Acquisition in human infants</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=17" title="Edit section: Acquisition in human infants">edit</a>]</div> The establishment of a gut flora is crucial to the health of an adult, as well as the functioning of the gastrointestinal tract.<a href="#cite_note-62">[62]</a> In humans, a gut flora similar to an adult's is formed within one to two years of birth as microbiota are acquired through parent-to-child transmission and transfer from food, water, and other environmental sources.<a href="#cite_note-63">[63]</a><a href="#cite_note-Sommer2013rev-12">[12]</a> <figure typeof="mw:File/Thumb"><a href="/wiki/File:Illustration_of_the_developmental_colonization_of_gut_bacteria.jpg" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/6/60/Illustration_of_the_developmental_colonization_of_gut_bacteria.jpg/500px-Illustration_of_the_developmental_colonization_of_gut_bacteria.jpg" decoding="async" width="500" height="226" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/6/60/Illustration_of_the_developmental_colonization_of_gut_bacteria.jpg/750px-Illustration_of_the_developmental_colonization_of_gut_bacteria.jpg 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/6/60/Illustration_of_the_developmental_colonization_of_gut_bacteria.jpg/1000px-Illustration_of_the_developmental_colonization_of_gut_bacteria.jpg 2x" data-file-width="2080" data-file-height="941" /></a><figcaption>Illustration showing the developmental colonization of gut microbiota</figcaption></figure> The traditional view of the <a href="/wiki/Gastrointestinal_tract" title="Gastrointestinal tract">gastrointestinal tract</a> of a normal <a href="/wiki/Fetus" title="Fetus">fetus</a> is that it is sterile, although this view has been challenged in the past few years.[<a href="/wiki/Wikipedia:Manual_of_Style/Words_to_watch#Relative_time_references" title="Wikipedia:Manual of Style/Words to watch">timeframe?</a>]<a href="#cite_note-64">[64]</a> Multiple lines of evidence have begun to emerge that suggest there may be bacteria in the intrauterine environment. In humans, research has shown that microbial colonization may occur in the fetus<a href="#cite_note-Matamoros2013-65">[65]</a> with one study showing Lactobacillus and Bifidobacterium species were present in placental biopsies.<a href="#cite_note-Mueller_109–117-66">[66]</a> Several <a href="/wiki/Animal_testing_on_rodents" title="Animal testing on rodents">rodent studies</a> have demonstrated the presence of bacteria in the amniotic fluid and placenta, as well as in the <a href="/wiki/Meconium" title="Meconium">meconium</a> of babies born by sterile cesarean section.<a href="#cite_note-67">[67]</a><a href="#cite_note-68">[68]</a> In another study, researchers administered a culture of bacteria orally to pregnant mice, and detected the bacteria in the offspring, likely resulting from transmission between the digestive tract and amniotic fluid via the blood stream.<a href="#cite_note-69">[69]</a> However, researchers caution that the source of these intrauterine bacteria, whether they are alive, and their role, is not yet understood.<a href="#cite_note-70">[70]</a><a href="#cite_note-Mueller_109–117-66">[66]</a> During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut.<a href="#cite_note-Sommer2013rev-12">[12]</a> The exact sources of bacteria are not fully understood, but may include the birth canal, other people (parents, siblings, hospital workers), breastmilk, food, and the general environment with which the infant interacts.<a href="#cite_note-71">[71]</a> Research has shown that the microbiome of babies born <a href="/wiki/Vaginal_delivery" title="Vaginal delivery">vaginally</a> differs significantly from that of babies delivered by <a href="/wiki/Caesarean_section" title="Caesarean section">caesarean section</a> and that vaginally born babies got most of their gut bacteria from their mother, while the microbiota of babies born by caesarean section had more bacteria associated with hospital environments.<a href="#cite_note-VaginalBirthMicrobiota-72">[72]</a> During the first year of life, the composition of the gut flora is generally simple and changes a great deal with time and is not the same across individuals.<a href="#cite_note-Sommer2013rev-12">[12]</a> The initial bacterial population are generally <a href="/wiki/Facultative_anaerobic_organism" title="Facultative anaerobic organism">facultative anaerobic organisms</a>; investigators believe that these initial colonizers decrease the oxygen concentration in the gut, which in turn allows obligately anaerobic bacteria like Bacteroidota, Actinomycetota, and Bacillota to become established and thrive.<a href="#cite_note-Sommer2013rev-12">[12]</a> Breast-fed babies become dominated by <a href="/wiki/Bifidobacteria" class="mw-redirect" title="Bifidobacteria">bifidobacteria</a>, possibly due to the contents of <a href="/wiki/Bifidus_factor" title="Bifidus factor">bifidobacterial growth factors</a> in breast milk, and by the fact that breast milk carries prebiotic components, allowing for healthy bacterial growth.<a href="#cite_note-Mueller_109–117-66">[66]</a><a href="#cite_note-73">[73]</a> Breast milk also contains higher levels of Immunoglobulin A (IgA) to help with the tolerance and regulation of the baby's immune system.<a href="#cite_note-74">[74]</a> In contrast, the microbiota of <a href="/wiki/Infant_formula" title="Infant formula">formula-fed</a> infants is more diverse, with high numbers of <a href="/wiki/Enterobacteriaceae" title="Enterobacteriaceae">Enterobacteriaceae</a>, <a href="/wiki/Enterococci" class="mw-redirect" title="Enterococci">enterococci</a>, bifidobacteria, Bacteroides, and clostridia.<a href="#cite_note-75">[75]</a> Caesarean section, <a href="/wiki/Antibiotic" title="Antibiotic">antibiotics</a>, and <a href="/wiki/Formula_feeding" class="mw-redirect" title="Formula feeding">formula feeding</a> may alter the gut microbiome composition.<a href="#cite_note-Mueller_109–117-66">[66]</a> Children treated with antibiotics have less stable, and less diverse floral communities.<a href="#cite_note-76">[76]</a> Caesarean sections have been shown to be disruptive to mother-offspring transmission of bacteria, which impacts the overall health of the offspring by raising risks of disease such as <a href="/wiki/Celiac_disease" class="mw-redirect" title="Celiac disease">celiac disease</a>, <a href="/wiki/Asthma" title="Asthma">asthma</a>, and <a href="/wiki/Type_1_diabetes" title="Type 1 diabetes">type 1 diabetes</a>.<a href="#cite_note-Mueller_109–117-66">[66]</a> This further evidences the importance of a healthy gut microbiome. Various methods of microbiome restoration are being explored, typically involving exposing the infant to maternal vaginal contents, and oral probiotics.<a href="#cite_note-Mueller_109–117-66">[66]</a> <div class="mw-heading mw-heading2"><h2 id="Functions">Functions</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=18" title="Edit section: Functions">edit</a>]</div> When the study of gut flora began in 1995,<a href="#cite_note-77">[77]</a> it was thought to have three key roles: direct defense against <a href="/wiki/Pathogen" title="Pathogen">pathogens</a>, fortification of host defense by its role in developing and maintaining the <a href="/wiki/Intestinal_epithelium" title="Intestinal epithelium">intestinal epithelium</a> and inducing antibody production there, and metabolizing otherwise indigestible compounds in food. Subsequent work discovered its role in training the developing immune system, and yet further work focused on its role in the <a href="/wiki/Gut%E2%80%93brain_axis" title="Gut–brain axis">gut–brain axis</a>.<a href="#cite_note-2014Wangrev-78">[78]</a> <div class="mw-heading mw-heading3"><h3 id="Direct_inhibition_of_pathogens">Direct inhibition of pathogens</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=19" title="Edit section: Direct inhibition of pathogens">edit</a>]</div> The gut flora community plays a direct role in defending against pathogens by fully colonising the space, making use of all available nutrients, and by secreting compounds known as <a href="/wiki/Cytokine" title="Cytokine">cytokines</a> that kill or inhibit unwelcome organisms that would compete for nutrients with it.<a href="#cite_note-Yoon2014rev-79">[79]</a> Different strains of gut bacteria cause the production of different cytokines. Cytokines are chemical compounds produced by our immune system for initiating the <a href="/wiki/Inflammatory_response" class="mw-redirect" title="Inflammatory response">inflammatory response</a> against infections. Disruption of the gut flora allows competing organisms like <a href="/wiki/Clostridioides_difficile_(bacteria)" class="mw-redirect" title="Clostridioides difficile (bacteria)">Clostridioides difficile</a> to become established that otherwise are kept in abeyance.<a href="#cite_note-Yoon2014rev-79">[79]</a> <div class="mw-heading mw-heading3"><h3 id="Development_of_enteric_protection_and_immune_system">Development of enteric protection and immune system</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=20" title="Edit section: Development of enteric protection and immune system">edit</a>]</div> <figure class="mw-default-size mw-halign-right" typeof="mw:File/Thumb"><a href="/wiki/File:Transvesicular_transport_by_microfold_cells.png" class="mw-file-description"><img src="//upload.wikimedia.org/wikipedia/commons/thumb/0/04/Transvesicular_transport_by_microfold_cells.png/220px-Transvesicular_transport_by_microfold_cells.png" decoding="async" width="220" height="218" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/0/04/Transvesicular_transport_by_microfold_cells.png/330px-Transvesicular_transport_by_microfold_cells.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/0/04/Transvesicular_transport_by_microfold_cells.png/440px-Transvesicular_transport_by_microfold_cells.png 2x" data-file-width="1223" data-file-height="1214" /></a><figcaption><a href="/wiki/Microfold_cells" class="mw-redirect" title="Microfold cells">Microfold cells</a> transfer antigens (Ag) from the lumen of the gut to <a href="/wiki/Gut-associated_lymphoid_tissue" title="Gut-associated lymphoid tissue">gut-associated lymphoid tissue</a> (GALT) via <a href="/wiki/Transcytosis" title="Transcytosis">transcytosis</a> and present them to different innate and adaptive immune cells.</figcaption></figure> In humans, a gut flora similar to an adult's is formed within one to two years of birth.<a href="#cite_note-Sommer2013rev-12">[12]</a> As the gut flora gets established, the lining of the intestines – the intestinal epithelium and the intestinal mucosal barrier that it secretes – develop as well, in a way that is tolerant to, and even supportive of, commensalistic microorganisms to a certain extent and also provides a barrier to pathogenic ones.<a href="#cite_note-Sommer2013rev-12">[12]</a> Specifically, <a href="/wiki/Goblet_cell" title="Goblet cell">goblet cells</a> that produce the mucosa proliferate, and the mucosa layer thickens, providing an outside mucosal layer in which "friendly" microorganisms can anchor and feed, and an inner layer that even these organisms cannot penetrate.<a href="#cite_note-Sommer2013rev-12">[12]</a><a href="#cite_note-Faderl2015rev-13">[13]</a> Additionally, the development of <a href="/wiki/Gut-associated_lymphoid_tissue" title="Gut-associated lymphoid tissue">gut-associated lymphoid tissue</a> (GALT), which forms part of the intestinal epithelium and which detects and reacts to pathogens, appears and develops during the time that the gut flora develops and established.<a href="#cite_note-Sommer2013rev-12">[12]</a> The GALT that develops is tolerant to gut flora species, but not to other microorganisms.<a href="#cite_note-Sommer2013rev-12">[12]</a> GALT also normally becomes tolerant to food to which the infant is exposed, as well as digestive products of food, and gut flora's <a href="/wiki/Metabolites" class="mw-redirect" title="Metabolites">metabolites</a> (molecules formed from metabolism) produced from food.<a href="#cite_note-Sommer2013rev-12">[12]</a> The human <a href="/wiki/Immune_system" title="Immune system">immune system</a> creates <a href="/wiki/Cytokine" title="Cytokine">cytokines</a> that can drive the immune system to produce inflammation in order to protect itself, and that can tamp down the immune response to maintain <a href="/wiki/Homeostasis" title="Homeostasis">homeostasis</a> and allow healing after insult or injury.<a href="#cite_note-Sommer2013rev-12">[12]</a> Different bacterial species that appear in gut flora have been shown to be able to drive the immune system to create cytokines selectively; for example <a href="/wiki/Bacteroides_fragilis" title="Bacteroides fragilis">Bacteroides fragilis</a> and some <a href="/wiki/Clostridia" title="Clostridia">Clostridia</a> species appear to drive an anti-inflammatory response, while some <a href="/wiki/Segmented_filamentous_bacteria" title="Segmented filamentous bacteria">segmented filamentous bacteria</a> drive the production of inflammatory cytokines.<a href="#cite_note-Sommer2013rev-12">[12]</a><a href="#cite_note-80">[80]</a> Gut flora can also regulate the production of <a href="/wiki/Antibodies" class="mw-redirect" title="Antibodies">antibodies</a> by the immune system.<a href="#cite_note-Sommer2013rev-12">[12]</a><a href="#cite_note-81">[81]</a> One function of this regulation is to cause <a href="/wiki/B_cells" class="mw-redirect" title="B cells">B cells</a> to class switch to <a href="/wiki/IgA" class="mw-redirect" title="IgA">IgA</a>. In most cases B cells need activation from <a href="/wiki/T_helper_cells" class="mw-redirect" title="T helper cells">T helper cells</a> to induce <a href="/wiki/Class_switching" class="mw-redirect" title="Class switching">class switching</a>; however, in another pathway, gut flora cause <a href="/wiki/NF-kB" class="mw-redirect" title="NF-kB">NF-kB</a> signaling by intestinal epithelial cells which results in further signaling molecules being secreted.<a href="#cite_note-Peterson-82">[82]</a> These signaling molecules interact with B cells to induce class switching to IgA.<a href="#cite_note-Peterson-82">[82]</a> IgA is an important type of antibody that is used in mucosal environments like the gut. It has been shown that IgA can help diversify the gut community and helps in getting rid of bacteria that cause inflammatory responses.<a href="#cite_note-Honda-83">[83]</a> Ultimately, IgA maintains a healthy environment between the host and gut bacteria.<a href="#cite_note-Honda-83">[83]</a> These cytokines and antibodies can have effects outside the gut, in the lungs and other tissues.<a href="#cite_note-Sommer2013rev-12">[12]</a> The immune system can also be altered due to the gut bacteria's ability to produce <a href="/wiki/Metabolites" class="mw-redirect" title="Metabolites">metabolites</a> that can affect cells in the immune system. For example <a href="/wiki/Short-chain_fatty_acid" title="Short-chain fatty acid">short-chain fatty acids</a> (SCFA) can be produced by some gut bacteria through <a href="/wiki/Fermentation" title="Fermentation">fermentation</a>.<a href="#cite_note-Levy-84">[84]</a> SCFAs stimulate a rapid increase in the production of innate immune cells like <a href="/wiki/Neutrophils" class="mw-redirect" title="Neutrophils">neutrophils</a>, <a href="/wiki/Basophils" class="mw-redirect" title="Basophils">basophils</a> and <a href="/wiki/Eosinophils" class="mw-redirect" title="Eosinophils">eosinophils</a>.<a href="#cite_note-Levy-84">[84]</a> These cells are part of the innate immune system that try to limit the spread of infection. <div class="mw-heading mw-heading3"><h3 id="Metabolism">Metabolism</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=21" title="Edit section: Metabolism">edit</a>]</div> <div class="skin-invert-image"> <table role="presentation" cellpadding="0" 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alt="Tryptophan metabolism diagram" src="//upload.wikimedia.org/wikipedia/commons/thumb/d/d0/Microbiota-derived_3-Indolepropionic_acid-notext.svg/600px-Microbiota-derived_3-Indolepropionic_acid-notext.svg.png" decoding="async" width="600" height="470" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/d/d0/Microbiota-derived_3-Indolepropionic_acid-notext.svg/900px-Microbiota-derived_3-Indolepropionic_acid-notext.svg.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/d/d0/Microbiota-derived_3-Indolepropionic_acid-notext.svg/1200px-Microbiota-derived_3-Indolepropionic_acid-notext.svg.png 2x" data-file-width="705" data-file-height="552" /></a> </div> <div style="text-align:left; font-size:14px; line-height:110%"> <div style="background-color:transparent; color:black"><div id="annotation_205x3" style="position:absolute; left:205px; top:3px; line-height:110%;"><a href="/wiki/Tryptophan" title="Tryptophan">Tryptophan</a></div> <div id="annotation_127x65" style="position:absolute; left:127px; top:65px; font-size:12px; font-size:12; line-height:14px;"><a href="/wiki/Clostridium_sporogenes" title="Clostridium sporogenes">Clostridium sporogenes</a></div> <div id="annotation_252x85" style="position:absolute; left:252px; top:85px; font-size:12px; font-size:12; line-height:14px;"><a href="/wiki/Lactobacillaceae" title="Lactobacillaceae">Lacto- bacilli</a></div> <div id="annotation_292x60" style="position:absolute; left:292px; top:60px; font-size:12px; font-size:12; line-height:14px; text-align:center;"><a href="/wiki/Tryptophanase" title="Tryptophanase">Tryptophanase</a>- expressing bacteria</div> <div id="annotation_148x116" style="position:absolute; left:148px; top:116px; font-size:14px; font-size:14; line-height:16px;"><a href="/wiki/3-Indolepropionic_acid" title="3-Indolepropionic acid">IPA</a></div> <div id="annotation_236x131" style="position:absolute; left:236px; top:131px; font-size:14px; font-size:14; line-height:16px;"><a href="/wiki/Indole-3-carbaldehyde" title="Indole-3-carbaldehyde">I3A</a></div> <div id="annotation_318x115" style="position:absolute; left:318px; top:115px; font-size:14px; font-size:14; line-height:16px;"><a href="/wiki/Indole" title="Indole">Indole</a></div> <div id="annotation_470x174" style="position:absolute; left:470px; top:174px; font-size:18px; font-size:18; line-height:20px; text-align:center;"><a href="/wiki/Liver" title="Liver">Liver</a></div> <div id="annotation_37x301" style="position:absolute; left:37px; top:301px; font-size:18px; font-size:18; line-height:20px;"><a href="/wiki/Human_brain" title="Human brain">Brain</a></div> <div id="annotation_133x352" style="position:absolute; left:133px; top:352px; font-size:14px; font-size:14; line-height:16px;"><a href="/wiki/3-Indolepropionic_acid" title="3-Indolepropionic acid">IPA</a></div> <div id="annotation_236x299" style="position:absolute; left:236px; top:299px; font-size:14px; font-size:14; line-height:16px;"><a href="/wiki/Indole-3-carbaldehyde" title="Indole-3-carbaldehyde">I3A</a></div> <div id="annotation_328x269" style="position:absolute; left:328px; top:269px; font-size:14px; font-size:14; line-height:16px;"><a href="/wiki/Indole" title="Indole">Indole</a></div> <div id="annotation_413x261" style="position:absolute; left:413px; top:261px; font-size:12px; font-size:12; line-height:14px; text-align:center;"><a href="/wiki/Indoxyl_sulfate" title="Indoxyl sulfate">Indoxyl sulfate</a></div> <div id="annotation_350x318" style="position:absolute; left:350px; top:318px; font-size:14px; font-size:14; line-height:16px;"><a href="/wiki/Activated_charcoal" class="mw-redirect" title="Activated charcoal">AST-120</a></div> <div id="annotation_281x346" style="position:absolute; left:281px; top:346px; font-size:12px; font-size:12; line-height:14px;"><a href="/wiki/Aryl_hydrocarbon_receptor" title="Aryl hydrocarbon receptor">AhR</a></div> <div id="annotation_269x297" style="position:absolute; left:269px; top:297px; font-size:11px; font-size:11; line-height:13px; text-align:center;">Intestinal <a href="/wiki/Immune_cells" class="mw-redirect" title="Immune cells">immune cells</a></div> <div id="annotation_40x209" style="position:absolute; left:40px; top:209px; font-size:18px; font-size:18; line-height:20px; text-align:center;"><a href="/wiki/Intestinal_epithelium" title="Intestinal epithelium">Intestinal epithelium</a></div> <div id="annotation_161.5x231" style="position:absolute; left:161.5px; top:231px; font-size:11px; font-size:11; line-height:13px;"><a href="/wiki/Pregnane_X_receptor" title="Pregnane X receptor">PXR</a></div> <div id="annotation_144x255" style="position:absolute; left:144px; top:255px; font-size:10px; font-size:10; line-height:12px;">Mucosal homeostasis: ↓<a href="/wiki/Tumor_necrosis_factor_alpha" class="mw-redirect" title="Tumor necrosis factor alpha">TNF-α</a> ↑<a href="/wiki/Tight_junction" title="Tight junction">Junction</a> protein- coding <a href="/wiki/Messenger_RNA" title="Messenger RNA">mRNAs</a></div> <div id="annotation_252.5x237" style="position:absolute; left:252.5px; top:237px; font-size:12px; font-size:12; line-height:14px;"><a href="/wiki/Enteroendocrine_cell#L_cell" title="Enteroendocrine cell">L cell</a></div> <div id="annotation_249x265" style="position:absolute; left:249px; top:265px; font-size:12px; font-size:12; line-height:14px;"><a href="/wiki/Glucagon-like_peptide-1" title="Glucagon-like peptide-1">GLP-1</a></div> <div id="annotation_335x227" style="position:absolute; left:335px; top:227px; font-size:12px; font-size:12; line-height:14px;"><a href="/wiki/Tight_junction" title="Tight junction">T J</a></div> <div id="annotation_15x390" style="position:absolute; left:15px; top:390px; font-size:10px; font-size:10; line-height:12px;"><a href="/wiki/Neuroprotectant" class="mw-redirect" title="Neuroprotectant">Neuroprotectant</a>: ↓Activation of <a href="/wiki/Glia" title="Glia">glial cells</a> and <a href="/wiki/Astrocyte" title="Astrocyte">astrocytes</a> ↓<a href="/wiki/4-Hydroxy-2-nonenal" class="mw-redirect" title="4-Hydroxy-2-nonenal">4-Hydroxy-2-nonenal</a> levels ↓<a href="/wiki/DNA_damage" class="mw-redirect" title="DNA damage">DNA damage</a> –<a href="/wiki/Antioxidant" title="Antioxidant">Antioxidant</a> –Inhibits <a href="/wiki/%CE%92-amyloid" class="mw-redirect" title="Β-amyloid">β-amyloid</a> fibril formation</div> <div id="annotation_243x370" style="position:absolute; left:243px; top:370px; font-size:10px; font-size:10; line-height:12px;">Maintains mucosal reactivity: ↑<a href="/wiki/Interleukin_22" title="Interleukin 22">IL-22</a> production</div> <div id="annotation_458x290" style="position:absolute; left:458px; top:290px; font-size:10px; font-size:10; line-height:12px;">Associated with <a href="/wiki/Vascular_disease" title="Vascular disease">vascular disease</a>: ↑<a href="/wiki/Oxidative_stress" title="Oxidative stress">Oxidative stress</a> ↑<a href="/wiki/Smooth_muscle_cell" class="mw-redirect" title="Smooth muscle cell">Smooth muscle cell</a> <a href="/wiki/Cell_proliferation" title="Cell proliferation">proliferation</a> ↑<a href="/wiki/Aorta" title="Aorta">Aortic wall</a> thickness and <a href="/wiki/Aortic_calcification" class="mw-redirect" title="Aortic calcification">calcification</a></div> <div id="annotation_458x391" style="position:absolute; left:458px; top:391px; font-size:10px; font-size:10; line-height:12px;">Associated with <a href="/wiki/Chronic_kidney_disease" title="Chronic kidney disease">chronic kidney disease</a>: ↑<a href="/wiki/Renal_dysfunction" class="mw-redirect" title="Renal dysfunction">Renal dysfunction</a> –<a href="/wiki/Uremic_toxin" class="mw-redirect" title="Uremic toxin">Uremic toxin</a></div> <div id="annotation_381x448" style="position:absolute; left:381px; top:448px; font-size:18px; font-size:18; line-height:20px;"><a href="/wiki/Kidney" title="Kidney">Kidneys</a></div></div> </div> </div> <div class="thumbcaption" style="clear:left"><div style="float:left;margin-right:0.5em"><img alt="The image above contains clickable links" src="//upload.wikimedia.org/wikipedia/commons/thumb/e/e6/Interactive_icon.svg/18px-Interactive_icon.svg.png" decoding="async" width="18" height="27" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/e/e6/Interactive_icon.svg/27px-Interactive_icon.svg.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/e/e6/Interactive_icon.svg/36px-Interactive_icon.svg.png 2x" data-file-width="133" data-file-height="200" /></div>This diagram shows the biosynthesis of <a href="/wiki/Bioactive_compound" title="Bioactive compound">bioactive compounds</a> (<a href="/wiki/Indole" title="Indole">indole</a> and certain other derivatives) from <a href="/wiki/Tryptophan" title="Tryptophan">tryptophan</a> by bacteria in the gut.<a href="#cite_note-Microbial_biosynthesis_of_bioactive_compounds-85">[85]</a> Indole is produced from tryptophan by bacteria that express <a href="/wiki/Tryptophanase" title="Tryptophanase">tryptophanase</a>.<a href="#cite_note-Microbial_biosynthesis_of_bioactive_compounds-85">[85]</a> <a href="/wiki/Clostridium_sporogenes" title="Clostridium sporogenes">Clostridium sporogenes</a> metabolizes tryptophan into indole and subsequently <a href="/wiki/3-Indolepropionic_acid" title="3-Indolepropionic acid">3-indolepropionic acid</a> (IPA),<a href="#cite_note-Microbiome_IPA-86">[86]</a> a highly potent <a href="/wiki/Neuroprotective" class="mw-redirect" title="Neuroprotective">neuroprotective</a> <a href="/wiki/Antioxidant" title="Antioxidant">antioxidant</a> that scavenges <a href="/wiki/Hydroxyl_radical" title="Hydroxyl radical">hydroxyl radicals</a>.<a href="#cite_note-Microbial_biosynthesis_of_bioactive_compounds-85">[85]</a><a href="#cite_note-Human_metabolome_IPA-87">[87]</a><a href="#cite_note-Indolepropionic_acid_scavenging-88">[88]</a> IPA binds to the <a href="/wiki/Pregnane_X_receptor" title="Pregnane X receptor">pregnane X receptor</a> (PXR) in intestinal cells, thereby facilitating mucosal homeostasis and <a href="/wiki/Intestinal_permeability" title="Intestinal permeability">barrier function</a>.<a href="#cite_note-Microbial_biosynthesis_of_bioactive_compounds-85">[85]</a> Following <a href="/wiki/Absorption_(pharmacokinetics)" class="mw-redirect" title="Absorption (pharmacokinetics)">absorption</a> from the intestine and <a href="/wiki/Distribution_(pharmacology)" title="Distribution (pharmacology)">distribution</a> to the brain, IPA confers a neuroprotective effect against <a href="/wiki/Cerebral_ischemia" class="mw-redirect" title="Cerebral ischemia">cerebral ischemia</a> and <a href="/wiki/Alzheimer%27s_disease" title="Alzheimer's disease">Alzheimer's disease</a>.<a href="#cite_note-Microbial_biosynthesis_of_bioactive_compounds-85">[85]</a> <a href="/wiki/Lactobacillaceae" title="Lactobacillaceae">Lactobacillaceae</a> (Lactobacillus <a href="/wiki/Sensu" title="Sensu">s.l.</a>) species metabolize tryptophan into <a href="/wiki/Indole-3-carboxaldehyde" class="mw-redirect" title="Indole-3-carboxaldehyde">indole-3-aldehyde</a> (I3A) which acts on the <a href="/wiki/Aryl_hydrocarbon_receptor" title="Aryl hydrocarbon receptor">aryl hydrocarbon receptor</a> (AhR) in intestinal immune cells, in turn increasing <a href="/wiki/Interleukin-22" class="mw-redirect" title="Interleukin-22">interleukin-22</a> (IL-22) production.<a href="#cite_note-Microbial_biosynthesis_of_bioactive_compounds-85">[85]</a> Indole itself <a href="/wiki/Secretagogue" title="Secretagogue">triggers the secretion</a> of <a href="/wiki/Glucagon-like_peptide-1" title="Glucagon-like peptide-1">glucagon-like peptide-1</a> (GLP-1) in <a href="/wiki/Enteroendocrine_cell#L_cell" title="Enteroendocrine cell">intestinal L cells</a> and acts as a <a href="/wiki/Ligand_(biochemistry)" title="Ligand (biochemistry)">ligand</a> for AhR.<a href="#cite_note-Microbial_biosynthesis_of_bioactive_compounds-85">[85]</a> Indole can also be metabolized by the liver into <a href="/wiki/Indoxyl_sulfate" title="Indoxyl sulfate">indoxyl sulfate</a>, a compound that is toxic in high concentrations and associated with <a href="/wiki/Vascular_disease" title="Vascular disease">vascular disease</a> and <a href="/wiki/Renal_dysfunction" class="mw-redirect" title="Renal dysfunction">renal dysfunction</a>.<a href="#cite_note-Microbial_biosynthesis_of_bioactive_compounds-85">[85]</a> AST-120 (<a href="/wiki/Activated_charcoal" class="mw-redirect" title="Activated charcoal">activated charcoal</a>), an intestinal <a href="/wiki/Sorbent" title="Sorbent">sorbent</a> that is <a href="/wiki/Oral_administration" title="Oral administration">taken by mouth</a>, <a href="/wiki/Adsorption" title="Adsorption">adsorbs</a> indole, in turn decreasing the concentration of indoxyl sulfate in blood plasma.<a href="#cite_note-Microbial_biosynthesis_of_bioactive_compounds-85">[85]</a></div> </div> </div> </td></tr></tbody></table></div> Without gut flora, the human body would be unable to utilize some of the undigested <a href="/wiki/Carbohydrate" title="Carbohydrate">carbohydrates</a> it consumes, because some types of gut flora have <a href="/wiki/Enzyme" title="Enzyme">enzymes</a> that human cells lack for breaking down certain <a href="/wiki/Polysaccharide" title="Polysaccharide">polysaccharides</a>.<a href="#cite_note-Clarke2014rev-14">[14]</a> Rodents raised in a <a href="/wiki/Asepsis" title="Asepsis">sterile</a> environment and lacking in gut flora need to eat 30% more <a href="/wiki/Calorie_(food)" class="mw-redirect" title="Calorie (food)">calories</a> just to remain the same weight as their normal counterparts.<a href="#cite_note-Clarke2014rev-14">[14]</a> Carbohydrates that humans cannot <a href="/wiki/Digestion" title="Digestion">digest</a> without bacterial help include certain <a href="/wiki/Starch_(food)" class="mw-redirect" title="Starch (food)">starches</a>, <a href="/wiki/Fiber_(food)" class="mw-redirect" title="Fiber (food)">fiber</a>, <a href="/wiki/Oligosaccharides" class="mw-redirect" title="Oligosaccharides">oligosaccharides</a>, and <a href="/wiki/Sugar" title="Sugar">sugars</a> that the body failed to digest and absorb like <a href="/wiki/Lactose" title="Lactose">lactose</a> in the case of <a href="/wiki/Lactose_intolerance" title="Lactose intolerance">lactose intolerance</a> and <a href="/wiki/Sugar_alcohol" title="Sugar alcohol">sugar alcohols</a>, <a href="/wiki/Mucus" title="Mucus">mucus</a> produced by the gut, and proteins.<a href="#cite_note-Quigley2013rev-9">[9]</a><a href="#cite_note-Clarke2014rev-14">[14]</a> Bacteria turn carbohydrates they ferment into <a href="/wiki/Short-chain_fatty_acid" title="Short-chain fatty acid">short-chain fatty acids</a> by a form of fermentation called <a href="/w/index.php?title=Saccharolytic_fermentation&action=edit&redlink=1" class="new" title="Saccharolytic fermentation (page does not exist)">saccharolytic fermentation</a>.<a href="#cite_note-gibson-47">[47]</a> Products include <a href="/wiki/Acetic_acid" title="Acetic acid">acetic acid</a>, <a href="/wiki/Propionic_acid" title="Propionic acid">propionic acid</a> and <a href="/wiki/Butyric_acid" title="Butyric acid">butyric acid</a>.<a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a><a href="#cite_note-gibson-47">[47]</a> These materials can be used by host cells, providing a major source of energy and nutrients.<a href="#cite_note-gibson-47">[47]</a> Gases (which are involved in <a href="/wiki/Gaseous_signaling_molecules" title="Gaseous signaling molecules">signaling</a><a href="#cite_note-89">[89]</a> and may cause <a href="/wiki/Flatulence" title="Flatulence">flatulence</a>) and <a href="/wiki/Organic_acid" title="Organic acid">organic acids</a>, such as <a href="/wiki/Lactic_acid" title="Lactic acid">lactic acid</a>, are also produced by fermentation.<a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a> Acetic acid is used by <a href="/wiki/Muscle" title="Muscle">muscle</a>, propionic acid facilitates <a href="/wiki/Liver" title="Liver">liver</a> production of <a href="/wiki/Adenosine_triphosphate" title="Adenosine triphosphate">ATP</a>, and butyric acid provides energy to gut cells.<a href="#cite_note-gibson-47">[47]</a> Gut flora also synthesize vitamins like <a href="/wiki/Biotin" title="Biotin">biotin</a> and <a href="/wiki/Folate" title="Folate">folate</a>, and facilitate absorption of <a href="/wiki/Dietary_minerals" class="mw-redirect" title="Dietary minerals">dietary minerals</a>, including magnesium, calcium, and iron.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a><a href="#cite_note-OHara06-25">[25]</a> <a href="/wiki/Methanobrevibacter_smithii" title="Methanobrevibacter smithii">Methanobrevibacter smithii</a> is unique because it is not a species of bacteria, but rather a member of <a href="/wiki/Domain_(taxonomy)" class="mw-redirect" title="Domain (taxonomy)">domain</a> <a href="/wiki/Archaea" title="Archaea">Archaea</a>, and is the most abundant <a href="/wiki/Methane" title="Methane">methane</a>-producing archaeal species in the human gastrointestinal microbiota.<a href="#cite_note-90">[90]</a> Gut microbiota also serve as a source of vitamins K and B12, which are not produced by the body or produced in little amount.<a href="#cite_note-91">[91]</a><a href="#cite_note-92">[92]</a> <div class="mw-heading mw-heading4"><h4 id="Cellulose_degradation">Cellulose degradation</h4>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=22" title="Edit section: Cellulose degradation">edit</a>]</div> Bacteria that degrade cellulose (such as <a href="/wiki/Ruminococcus" title="Ruminococcus">Ruminococcus</a>) are prevalent among <a href="/wiki/Hominidae" title="Hominidae">great apes</a>, ancient human societies, <a href="/wiki/Hunter-gatherer" title="Hunter-gatherer">hunter-gatherer</a> communities, and even modern rural populations. However, they are rare in industrialized societies. Human-associated strains have acquired genes that can degrade specific plant fibers such as <a href="/wiki/Maize" title="Maize">maize</a>, <a href="/wiki/Rice" title="Rice">rice</a>, and <a href="/wiki/Wheat" title="Wheat">wheat</a>. Bacterial strains found in primates can also degrade <a href="/wiki/Chitin" title="Chitin">chitin</a>, a polymer abundant in insects, which are part of the diet of many nonhuman <a href="/wiki/Primate" title="Primate">primates</a>. The decline of these bacteria in the human gut were likely influenced by the shift toward western lifestyles.<a href="#cite_note-93">[93]</a> <div class="mw-heading mw-heading4"><h4 id="Pharmacomicrobiomics">Pharmacomicrobiomics</h4>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=23" title="Edit section: Pharmacomicrobiomics">edit</a>]</div> The human <a href="/wiki/Metagenomics" title="Metagenomics">metagenome</a> (i.e., the genetic composition of an individual and all microorganisms that reside on or within the individual's body) varies considerably between individuals.<a href="#cite_note-Pharmacomicrobiomics-94">[94]</a><a href="#cite_note-Human_microbiome-95">[95]</a> Since the total number of microbial cells in the human body (over 100 trillion) greatly outnumbers Homo sapiens cells (tens of trillions),<a href="#cite_note-96">[note 1]</a><a href="#cite_note-Pharmacomicrobiomics-94">[94]</a><a href="#cite_note-Gut_feeling-97">[96]</a> there is considerable potential for interactions between drugs and an individual's microbiome, including: drugs altering the composition of the <a href="/wiki/Human_microbiome" title="Human microbiome">human microbiome</a>, <a href="/wiki/Drug_metabolism" title="Drug metabolism">drug metabolism</a> by microbial enzymes modifying the drug's <a href="/wiki/Pharmacokinetic" class="mw-redirect" title="Pharmacokinetic">pharmacokinetic</a> profile, and microbial drug metabolism affecting a drug's clinical efficacy and <a href="/wiki/Toxicity" title="Toxicity">toxicity</a> profile.<a href="#cite_note-Pharmacomicrobiomics-94">[94]</a><a href="#cite_note-Human_microbiome-95">[95]</a><a href="#cite_note-Microbial_amphetamine_metabolism_-_E._coli-98">[97]</a> Apart from carbohydrates, gut microbiota can also metabolize other <a href="/wiki/Xenobiotic" title="Xenobiotic">xenobiotics</a> such as drugs, <a href="/wiki/Phytochemical" title="Phytochemical">phytochemicals</a>, and food toxicants. More than 30 drugs have been shown to be metabolized by gut microbiota.<a href="#cite_note-99">[98]</a> The microbial metabolism of drugs can sometimes inactivate the drug.<a href="#cite_note-100">[99]</a> <div class="mw-heading mw-heading5"><h5 id="Contribution_to_drug_metabolism">Contribution to drug metabolism</h5>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=24" title="Edit section: Contribution to drug metabolism">edit</a>]</div> The gut microbiota is an enriched community that contains diverse genes with huge biochemical capabilities to modify drugs, especially those taken by mouth.<a href="#cite_note-:8-101">[100]</a> Gut microbiota can affect drug metabolism via direct and indirect mechanisms.<a href="#cite_note-Spanogiannopoulos_273–287-102">[101]</a> The direct mechanism is mediated by the microbial enzymes that can modify the chemical structure of the administered drugs.<a href="#cite_note-Maini_Rekdal-103">[102]</a> Conversely, the indirect pathway is mediated by the microbial metabolites which affect the expression of host metabolizing enzymes such as <a href="/wiki/Cytochrome_P450" title="Cytochrome P450">cytochrome P450</a>.<a href="#cite_note-Dempsey_481–490-104">[103]</a><a href="#cite_note-Spanogiannopoulos_273–287-102">[101]</a> The effects of the gut microbiota on the pharmacokinetics and bioavailability of the drug have been investigated a few decades ago.<a href="#cite_note-105">[104]</a><a href="#cite_note-Dobkin_325–327-106">[105]</a><a href="#cite_note-107">[106]</a> These effects can be varied; it could activate the inactive drugs such as lovastatin,<a href="#cite_note-Yoo_1508–1513-108">[107]</a> inactivate the active drug such as <a href="/wiki/Digoxin" title="Digoxin">digoxin</a><a href="#cite_note-109">[108]</a> or induce drug toxicity as in <a href="/wiki/Irinotecan" title="Irinotecan">irinotecan</a>.<a href="#cite_note-110">[109]</a> Since then, the impacts of the gut microbiota on the pharmacokinetics of many drugs were heavily studied.<a href="#cite_note-:9-111">[110]</a><a href="#cite_note-:8-101">[100]</a> The human gut microbiota plays a crucial role in modulating the effect of the administered drugs on the human. Directly, gut microbiota can synthesize and release a series of enzymes with the capability to metabolize drugs such as microbial biotransformation of L-dopa by decarboxylase and dehydroxylase enzymes.<a href="#cite_note-Maini_Rekdal-103">[102]</a> On the contrary, gut microbiota may also alter the metabolism of the drugs by modulating the host drug metabolism. This mechanism can be mediated by microbial metabolites or by modifying host metabolites which in turn change the expression of host metabolizing enzymes.<a href="#cite_note-Dempsey_481–490-104">[103]</a> A large number of studies have demonstrated the metabolism of over 50 drugs by the gut microbiota.<a href="#cite_note-:9-111">[110]</a><a href="#cite_note-Spanogiannopoulos_273–287-102">[101]</a> For example, lovastatin (a cholesterol-lowering agent) which is a lactone prodrug is partially activated by the human gut microbiota forming active acid hydroxylated metabolites.<a href="#cite_note-Yoo_1508–1513-108">[107]</a> Conversely, digoxin (a drug used to treat Congestive Heart Failure) is inactivated by a member of the gut microbiota (i.e. Eggerthella lanta).<a href="#cite_note-:0-112">[111]</a> Eggerthella lanta has a cytochrome-encoding operon up-regulated by digoxin and associated with digoxin-inactivation.<a href="#cite_note-:0-112">[111]</a> Gut microbiota can also modulate the efficacy and toxicity of chemotherapeutic agents such as irinotecan.<a href="#cite_note-113">[112]</a> This effect is derived from the microbiome-encoded β-glucuronidase enzymes which recover the active form of the irinotecan causing gastrointestinal toxicity.<a href="#cite_note-114">[113]</a> <div class="mw-heading mw-heading5"><h5 id="Secondary_metabolites">Secondary metabolites</h5>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=25" title="Edit section: Secondary metabolites">edit</a>]</div> This microbial community in the gut has a huge biochemical capability to produce distinct secondary metabolites that are sometimes produced from the metabolic conversion of dietary foods such as <a href="/wiki/Fiber" title="Fiber">fibers</a>, endogenous biological compounds such as <a href="/wiki/Indole" title="Indole">indole</a> or <a href="/wiki/Bile_acid" title="Bile acid">bile acids</a>.<a href="#cite_note-115">[114]</a><a href="#cite_note-116">[115]</a><a href="#cite_note-Collins_et_al_Bile_acids_and_the_gut_microbiota-117">[116]</a> Microbial metabolites especially short chain fatty acids (SCFAs) and secondary bile acids (BAs) play important roles for the human in health and disease states.<a href="#cite_note-118">[117]</a><a href="#cite_note-119">[118]</a><a href="#cite_note-:7-120">[119]</a> One of the most important bacterial metabolites produced by the gut microbiota is secondary bile acids (BAs).<a href="#cite_note-Collins_et_al_Bile_acids_and_the_gut_microbiota-117">[116]</a> These metabolites are produced by the bacterial biotransformation of the primary bile acids such as cholic acid (CA) and chenodeoxycholic acid (CDCA) into secondary bile acids (BAs) lithocholic acid (LCA) and deoxy cholic acid (DCA) respectively.<a href="#cite_note-:6-121">[120]</a> Primary bile acids which are synthesized by hepatocytes and stored in the gall bladder possess hydrophobic characters. These metabolites are subsequently metabolized by the gut microbiota into secondary metabolites with increased hydrophobicity.<a href="#cite_note-:6-121">[120]</a> Bile salt hydrolases (BSH) which are conserved across gut microbiota phyla such as Bacteroides, Firmicutes, and Actinobacteria responsible for the first step of secondary bile acids metabolism.<a href="#cite_note-:6-121">[120]</a> Secondary bile acids (BAs) such as DCA and LCA have been demonstrated to inhibit both Clostridioides difficile germination and outgrowth.<a href="#cite_note-:7-120">[119]</a> <div class="mw-heading mw-heading4"><h4 id="Dysbiosis">Dysbiosis</h4>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=26" title="Edit section: Dysbiosis">edit</a>]</div> The gut microbiota is important for maintaining homeostasis in the intestine. Development of <a href="/wiki/Gastrointestinal_cancer" title="Gastrointestinal cancer">intestinal cancer</a> is associated with an imbalance in the natural microflora (dysbiosis).<a href="#cite_note-Cao2017-122">[121]</a> The secondary bile acid <a href="/wiki/Deoxycholic_acid" title="Deoxycholic acid">deoxycholic acid</a> is associated with alterations of the microbial community that lead to increased intestinal carcinogenesis.<a href="#cite_note-Cao2017-122">[121]</a> Increased exposure of the colon to secondary bile acids resulting from dysbiosis can cause <a href="/wiki/DNA_damage_(naturally_occurring)" title="DNA damage (naturally occurring)">DNA damage</a>, and such damage can produce carcinogenic mutations in cells of the colon.<a href="#cite_note-Bernstein2022-123">[122]</a> The high density of bacteria in the <a href="/wiki/Colon_(anatomy)" class="mw-redirect" title="Colon (anatomy)">colon</a> (about 1012 per ml.) that are subject to dysbiosis compared to the relatively low density in the <a href="/wiki/Small_intestine" title="Small intestine">small intestine</a> (about 102 per ml.) may account for the greater than 10-fold higher incidence of cancer in the colon compared to the small intestine.<a href="#cite_note-Bernstein2022-123">[122]</a> <div class="mw-heading mw-heading3"><h3 id="Gut–brain_axis">Gut–brain axis</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=27" title="Edit section: Gut–brain axis">edit</a>]</div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1236090951"><div role="note" class="hatnote navigation-not-searchable">Main article: <a href="/wiki/Gut%E2%80%93brain_axis" title="Gut–brain axis">Gut–brain axis</a></div> The gut microbiota contributes to digestion and immune modulation, as it plays a role in the gut-brain axis, where microbial metabolites such as short-chain fatty acids and neurotransmitters influence brain function and behavior. The gut–brain axis is the biochemical signaling that takes place between the <a href="/wiki/Gastrointestinal_tract" title="Gastrointestinal tract">gastrointestinal tract</a> and the <a href="/wiki/Central_nervous_system" title="Central nervous system">central nervous system</a>.<a href="#cite_note-2014Wangrev-78">[78]</a> That term has been expanded to include the role of the gut flora in the interplay; the term "microbiome––brain axis" is sometimes used to describe paradigms explicitly including the gut flora.<a href="#cite_note-2014Wangrev-78">[78]</a><a href="#cite_note-Mayer2014rev-124">[123]</a><a href="#cite_note-DinanandCryan2015-125">[124]</a> Broadly defined, the gut–brain axis includes the central nervous system, <a href="/wiki/Neuroendocrine_System" class="mw-redirect" title="Neuroendocrine System">neuroendocrine</a> and <a href="/wiki/Neuroimmune_system" title="Neuroimmune system">neuroimmune</a> systems including the <a href="/wiki/Hypothalamic%E2%80%93pituitary%E2%80%93adrenal_axis" title="Hypothalamic–pituitary–adrenal axis">hypothalamic–pituitary–adrenal axis</a> (HPA axis), sympathetic and parasympathetic arms of the <a href="/wiki/Autonomic_nervous_system" title="Autonomic nervous system">autonomic nervous system</a> including the <a href="/wiki/Enteric_nervous_system" title="Enteric nervous system">enteric nervous system</a>, the <a href="/wiki/Vagus_nerve" title="Vagus nerve">vagus nerve</a>, and the gut <a href="/wiki/Microbiota" title="Microbiota">microbiota</a>.<a href="#cite_note-2014Wangrev-78">[78]</a><a href="#cite_note-DinanandCryan2015-125">[124]</a> Studies show links between gut dysbiosis and mental health conditions, indicating a complex interaction that impacts mood and cognitive functions. A <a href="/wiki/Systematic_review" title="Systematic review">systematic review</a> from 2016 examined the preclinical and small human trials that have been conducted with certain commercially available strains of <a href="/wiki/Probiotic" title="Probiotic">probiotic</a> bacteria and found that among those tested, <a href="/wiki/Bifidobacterium" title="Bifidobacterium">Bifidobacterium</a> and Lactobacillus <a href="/wiki/Genera" class="mw-redirect" title="Genera">genera</a> (<a href="/wiki/B._longum" class="mw-redirect" title="B. longum">B. longum</a>, <a href="/wiki/B._breve" class="mw-redirect" title="B. breve">B. breve</a>, <a href="/wiki/B._infantis" class="mw-redirect" title="B. infantis">B. infantis</a>, <a href="/wiki/L._helveticus" class="mw-redirect" title="L. helveticus">L. helveticus</a>, <a href="/wiki/L._rhamnosus" class="mw-redirect" title="L. rhamnosus">L. rhamnosus</a>, <a href="/wiki/Lactobacillus_plantarum" class="mw-redirect" title="Lactobacillus plantarum">L. plantarum</a>, and <a href="/wiki/L._casei" class="mw-redirect" title="L. casei">L. casei</a>), had the most potential to be useful for certain <a href="/wiki/Central_nervous_system_disorder" class="mw-redirect" title="Central nervous system disorder">central nervous system disorders</a>.<a href="#cite_note-CNS_SystRev_2016-16">[16]</a> <div class="mw-heading mw-heading2"><h2 id="Alterations_in_microbiota_balance">Alterations in microbiota balance</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=28" title="Edit section: Alterations in microbiota balance">edit</a>]</div> <div class="mw-heading mw-heading3"><h3 id="Effects_of_antibiotic_use">Effects of antibiotic use</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=29" title="Edit section: Effects of antibiotic use">edit</a>]</div> Altering the numbers of gut bacteria, for example by taking <a href="/wiki/Broad-spectrum_antibiotic" title="Broad-spectrum antibiotic">broad-spectrum antibiotics</a>, may affect the host's health and ability to digest food.<a href="#cite_note-Carman-126">[125]</a> Antibiotics can cause <a href="/wiki/Antibiotic-associated_diarrhea" title="Antibiotic-associated diarrhea">antibiotic-associated diarrhea</a> by irritating the <a href="/wiki/Bowel" class="mw-redirect" title="Bowel">bowel</a> directly, changing the levels of microbiota, or allowing <a href="/wiki/Pathogen" title="Pathogen">pathogenic</a> bacteria to grow.<a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a> Another harmful effect of antibiotics is the increase in numbers of <a href="/wiki/Antibiotic-resistant_bacteria" class="mw-redirect" title="Antibiotic-resistant bacteria">antibiotic-resistant bacteria</a> found after their use, which, when they invade the host, cause illnesses that are difficult to treat with antibiotics.<a href="#cite_note-Carman-126">[125]</a> Changing the numbers and species of gut microbiota can reduce the body's ability to ferment carbohydrates and metabolize <a href="/wiki/Bile" title="Bile">bile</a> acids and may cause <a href="/wiki/Diarrhea" title="Diarrhea">diarrhea</a>. Carbohydrates that are not broken down may absorb too much water and cause runny stools, or lack of SCFAs produced by gut microbiota could cause diarrhea.<a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a> A reduction in levels of native bacterial species also disrupts their ability to inhibit the growth of harmful species such as C. difficile and Salmonella Kedougou, and these species can get out of hand, though their overgrowth may be incidental and not be the true cause of diarrhea.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a><a href="#cite_note-Beaugerie_L_and_Petit_JC-7">[7]</a><a href="#cite_note-Carman-126">[125]</a> Emerging treatment protocols for C. difficile infections involve fecal microbiota transplantation of donor feces (see <a href="/wiki/Fecal_transplant" class="mw-redirect" title="Fecal transplant">Fecal transplant</a>).<a href="#cite_note-127">[126]</a> Initial reports of treatment describe success rates of 90%, with few side effects. Efficacy is speculated to result from restoring bacterial balances of bacteroides and firmicutes classes of bacteria.<a href="#cite_note-Brandt-128">[127]</a> The composition of the gut microbiome also changes in severe illnesses, due not only to antibiotic use but also to such factors as <a href="/wiki/Ischemia" title="Ischemia">ischemia</a> of the gut, failure to eat, and <a href="/wiki/Immune_compromise" class="mw-redirect" title="Immune compromise">immune compromise</a>. Negative effects from this have led to interest in <a href="/w/index.php?title=Selective_digestive_tract_decontamination&action=edit&redlink=1" class="new" title="Selective digestive tract decontamination (page does not exist)">selective digestive tract decontamination</a>, a treatment to kill only pathogenic bacteria and allow the re-establishment of healthy ones.<a href="#cite_note-Knight-129">[128]</a> Antibiotics alter the population of the microbiota in the <a href="/wiki/Gastrointestinal_tract" title="Gastrointestinal tract">gastrointestinal tract</a>, and this may change the intra-community metabolic interactions, modify caloric intake by using carbohydrates, and globally affect host metabolic, hormonal, and immune homeostasis.<a href="#cite_note-cho2012-130">[129]</a> There is reasonable evidence that taking probiotics containing Lactobacillus species may help prevent antibiotic-associated diarrhea and that taking probiotics with Saccharomyces (e.g., <a href="/wiki/Saccharomyces_boulardii" title="Saccharomyces boulardii">Saccharomyces boulardii</a> ) may help to prevent Clostridioides difficile infection following systemic antibiotic treatment.<a href="#cite_note-JFP2016rev-131">[130]</a> <div class="mw-heading mw-heading3"><h3 id="Pregnancy">Pregnancy</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=30" title="Edit section: Pregnancy">edit</a>]</div> The gut microbiota of a woman changes as <a href="/wiki/Pregnancy" title="Pregnancy">pregnancy</a> advances, with the changes similar to those seen in <a href="/wiki/Metabolic_syndromes" class="mw-redirect" title="Metabolic syndromes">metabolic syndromes</a> such as diabetes. The change in gut microbiota causes no ill effects. The newborn's gut microbiota resemble the mother's first-trimester samples. The diversity of the microbiome decreases from the first to third trimester, as the numbers of certain species go up.<a href="#cite_note-Mueller_109–117-66">[66]</a><a href="#cite_note-132">[131]</a> <div class="mw-heading mw-heading3"><h3 id="Probiotics,_prebiotics,_synbiotics,_and_pharmabiotics">Probiotics, prebiotics, synbiotics, and pharmabiotics</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=31" title="Edit section: Probiotics, prebiotics, synbiotics, and pharmabiotics">edit</a>]</div> <a href="/wiki/Probiotics" class="mw-redirect" title="Probiotics">Probiotics</a> contain live <a href="/wiki/Microorganism" title="Microorganism">microorganisms</a>. When consumed, they are believed to provide health benefits by altering the microbiome composition.<a href="#cite_note-:10-133">[132]</a><a href="#cite_note-Expert-134">[133]</a><a href="#cite_note-bridging-135">[134]</a> Current research explores using probiotics as a way to restore the microbial balance of the <a href="/wiki/Gastrointestinal_tract" title="Gastrointestinal tract">intestine</a> by stimulating the immune system and inhibiting pro-inflammatory <a href="/wiki/Cytokine" title="Cytokine">cytokines</a>.<a href="#cite_note-:10-133">[132]</a> With regard to gut microbiota, <a href="/wiki/Prebiotics" class="mw-redirect" title="Prebiotics">prebiotics</a> are typically non-digestible, <a href="/wiki/Dietary_fiber" title="Dietary fiber">fiber</a> compounds that pass undigested through the upper part of the <a href="/wiki/Gastrointestinal_tract" title="Gastrointestinal tract">gastrointestinal tract</a> and stimulate the growth or activity of advantageous gut flora by acting as <a href="/wiki/Substrate_(biology)" title="Substrate (biology)">substrate</a> for them.<a href="#cite_note-gibson-47">[47]</a><a href="#cite_note-2015defRev-136">[135]</a> <a href="/wiki/Synbiotics" title="Synbiotics">Synbiotics</a> refers to <a href="/wiki/Food_ingredient" class="mw-redirect" title="Food ingredient">food ingredients</a> or <a href="/wiki/Dietary_supplements" class="mw-redirect" title="Dietary supplements">dietary supplements</a> combining probiotics and prebiotics in a form of <a href="/wiki/Synergy" title="Synergy">synergism</a>.<a href="#cite_note-137">[136]</a> The term "pharmabiotics" is used in various ways, to mean: <a href="/wiki/Pharmaceutical_formulation" title="Pharmaceutical formulation">pharmaceutical formulations</a> (standardized manufacturing that can obtain regulatory approval as a drug) of probiotics, <a href="/wiki/Prebiotics" class="mw-redirect" title="Prebiotics">prebiotics</a>, or <a href="/wiki/Synbiotics" title="Synbiotics">synbiotics</a>;<a href="#cite_note-138">[137]</a> probiotics that have been genetically engineered or otherwise optimized for best performance (shelf life, survival in the digestive tract, etc.);<a href="#cite_note-139">[138]</a> and the natural products of gut flora metabolism (vitamins, etc.).<a href="#cite_note-140">[139]</a> There is some evidence that treatment with some probiotic strains of bacteria may be effective in <a href="/wiki/Irritable_bowel_syndrome" title="Irritable bowel syndrome">irritable bowel syndrome</a>,<a href="#cite_note-141">[140]</a><a href="#cite_note-142">[141]</a> abdominal bloating <a href="#cite_note-143">[142]</a>and <a href="/wiki/Chronic_idiopathic_constipation" class="mw-redirect" title="Chronic idiopathic constipation">chronic idiopathic constipation</a>. Those organisms most likely to result in a decrease of symptoms have included: <ul><li><a href="/wiki/Bifidobacterium_breve" title="Bifidobacterium breve">Bifidobacterium breve</a></li> <li><a href="/wiki/Bifidobacterium_infantis" class="mw-redirect" title="Bifidobacterium infantis">Bifidobacterium infantis</a></li> <li><a href="/wiki/Enterococcus_faecium" title="Enterococcus faecium">Enterococcus faecium</a></li> <li><a href="/wiki/Lactobacillus_plantarum" class="mw-redirect" title="Lactobacillus plantarum">Lactobacillus plantarum</a></li> <li><a href="/wiki/Lactobacillus_reuteri" class="mw-redirect" title="Lactobacillus reuteri">Lactobacillus reuteri</a></li> <li><a href="/wiki/Lactobacillus_rhamnosus" class="mw-redirect" title="Lactobacillus rhamnosus">Lactobacillus rhamnosus</a></li> <li><a href="/wiki/Lactobacillus_salivarius" class="mw-redirect" title="Lactobacillus salivarius">Lactobacillus salivarius</a></li> <li><a href="/wiki/Propionibacterium_freudenreichii" title="Propionibacterium freudenreichii">Propionibacterium freudenreichii</a></li> <li><a href="/wiki/Saccharomyces_boulardii" title="Saccharomyces boulardii">Saccharomyces boulardii</a></li> <li><a href="/wiki/Escherichia_coli_Nissle_1917" title="Escherichia coli Nissle 1917">Escherichia coli Nissle 1917</a></li> <li><a href="/wiki/Streptococcus_thermophilus" title="Streptococcus thermophilus">Streptococcus thermophilus</a><a href="#cite_note-FordQuigley2014-144">[143]</a><a href="#cite_note-Ghouri2014-145">[144]</a><a href="#cite_note-146">[145]</a></li></ul> <div class="mw-heading mw-heading3"><h3 id="Fecal_floatation">Fecal floatation</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=32" title="Edit section: Fecal floatation">edit</a>]</div> Feces of about 10–15% of people consistently floats in toilet water ('floaters'), while the rest produce feces that sinks ('sinkers') and production of gas causes feces to float.<a href="#cite_note-147">[146]</a> While conventional mice often produce 'floaters', gnotobiotic germfree mice no gut microbiota (bred in germfree isolator) produce 'sinkers', and gut microbiota colonization in germfree mice leads to food transformation to microbial biomass and enrichment of multiple gasogenic bacterial species that turns the 'sinkers' into 'floaters'.<a href="#cite_note-148">[147]</a> <div class="mw-heading mw-heading3"><h3 id="Research">Research</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=33" title="Edit section: Research">edit</a>]</div> Tests for whether non-antibiotic drugs may impact human gut-associated bacteria were performed by <a href="/wiki/In_vitro" title="In vitro">in vitro</a> analysis on more than 1000 marketed drugs against 40 gut bacterial strains, demonstrating that 24% of the drugs inhibited the growth of at least one of the bacterial strains.<a href="#cite_note-149">[148]</a> <div class="mw-heading mw-heading3"><h3 id="Effects_of_exercise">Effects of exercise</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=34" title="Edit section: Effects of exercise">edit</a>]</div> Gut microbiota and exercise have recently been shown to be interconnected. Both moderate and intense exercise are typically part of the training regimen of endurance athletes, but they exert different effects on health. The interconnection between gut microbiota and endurance sports depends upon exercise intensity and training status.<a href="#cite_note-150">[149]</a> <div class="mw-heading mw-heading2"><h2 id="Role_in_disease">Role in disease</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=35" title="Edit section: Role in disease">edit</a>]</div> Bacteria in the digestive tract can contribute to and be affected by disease in various ways. The presence or overabundance of some kinds of bacteria may contribute to inflammatory disorders such as <a href="/wiki/Inflammatory_bowel_disease" title="Inflammatory bowel disease">inflammatory bowel disease</a>.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a> Additionally, metabolites from certain members of the gut flora may influence host signalling pathways, contributing to disorders such as <a href="/wiki/Obesity" title="Obesity">obesity</a> and <a href="/wiki/Colon_cancer" class="mw-redirect" title="Colon cancer">colon cancer</a>.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a> Some gut bacteria may also cause <a href="/wiki/Infection" title="Infection">infections</a> and <a href="/wiki/Sepsis" title="Sepsis">sepsis</a>, for example when they are allowed to <a href="/wiki/Intestinal_permeability" title="Intestinal permeability">pass from the gut into the rest of the body</a>.<a href="#cite_note-Guarner_and_Malagelada_2003b-6">[6]</a> <div class="mw-heading mw-heading3"><h3 id="Ulcers">Ulcers</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=36" title="Edit section: Ulcers">edit</a>]</div> <a href="/wiki/Helicobacter_pylori" title="Helicobacter pylori">Helicobacter pylori</a> infection can initiate formation of stomach ulcers when the bacteria penetrate the stomach epithelial lining, then causing an <a href="/wiki/Phagocytosis" title="Phagocytosis">inflammatory phagocytotic response</a>.<a href="#cite_note-kamboj-151">[150]</a> In turn, the inflammation damages parietal cells which release excessive <a href="/wiki/Hydrochloric_acid" title="Hydrochloric acid">hydrochloric acid</a> into the stomach and produce less of the protective mucus.<a href="#cite_note-hopkins-152">[151]</a> Injury to the stomach lining, leading to <a href="/wiki/Stomach_ulcer" class="mw-redirect" title="Stomach ulcer">ulcers</a>, develops when gastric acid overwhelms the defensive properties of cells and inhibits endogenous <a href="/wiki/Prostaglandin" title="Prostaglandin">prostaglandin</a> synthesis, reduces mucus and bicarbonate secretion, reduces mucosal blood flow, and lowers resistance to injury.<a href="#cite_note-hopkins-152">[151]</a> Reduced protective properties of the stomach lining increase vulnerability to further injury and ulcer formation by stomach acid, <a href="/wiki/Pepsin" title="Pepsin">pepsin</a>, and bile salts.<a href="#cite_note-kamboj-151">[150]</a><a href="#cite_note-hopkins-152">[151]</a> <div class="mw-heading mw-heading3"><h3 id="Bowel_perforation">Bowel perforation</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=37" title="Edit section: Bowel perforation">edit</a>]</div> Normally-<a href="/wiki/Commensalism" title="Commensalism">commensal bacteria</a> can harm the host if they extrude from the intestinal tract.<a href="#cite_note-Sommer2013rev-12">[12]</a><a href="#cite_note-Faderl2015rev-13">[13]</a> <a href="https://en.wiktionary.org/wiki/translocation" class="extiw" title="wikt:translocation">Translocation</a>, which occurs when bacteria leave the gut through its <a href="/wiki/Mucosa" class="mw-redirect" title="Mucosa">mucosal</a> lining, can occur in a number of different diseases.<a href="#cite_note-Faderl2015rev-13">[13]</a> If the gut is perforated, bacteria invade the <a href="/wiki/Interstitium" title="Interstitium">interstitium</a>, causing a potentially fatal <a href="/wiki/Infection" title="Infection">infection</a>.<a href="#cite_note-Prescotts-5">[5]</a>: 715  <div class="mw-heading mw-heading3"><h3 id="Inflammatory_bowel_diseases">Inflammatory bowel diseases</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=38" title="Edit section: Inflammatory bowel diseases">edit</a>]</div> The two main types of <a href="/wiki/Inflammatory_bowel_disease" title="Inflammatory bowel disease">inflammatory bowel diseases</a>, <a href="/wiki/Crohn%27s_disease" title="Crohn's disease">Crohn's disease</a> and <a href="/wiki/Ulcerative_colitis" title="Ulcerative colitis">ulcerative colitis</a>, are <a href="/wiki/Chronic_condition" title="Chronic condition">chronic</a> inflammatory disorders of the gut; the causes of these diseases are unknown and issues with the gut flora and its relationship with the host have been implicated in these conditions.<a href="#cite_note-Shen2016rev-15">[15]</a><a href="#cite_note-BurischJess2013-153">[152]</a><a href="#cite_note-154">[153]</a><a href="#cite_note-2016BoulangeRev-155">[154]</a> Additionally, it appears that interactions of gut flora with the gut–brain axis have a role in IBD, with physiological stress mediated through the <a href="/wiki/Hypothalamic%E2%80%93pituitary%E2%80%93adrenal_axis" title="Hypothalamic–pituitary–adrenal axis">hypothalamic–pituitary–adrenal axis</a> driving changes to intestinal epithelium and the gut flora in turn releasing factors and metabolites that trigger signaling in the <a href="/wiki/Enteric_nervous_system" title="Enteric nervous system">enteric nervous system</a> and the <a href="/wiki/Vagus_nerve" title="Vagus nerve">vagus nerve</a>.<a href="#cite_note-Saxena2016-4">[4]</a> The diversity of gut flora appears to be significantly diminished in people with inflammatory bowel diseases compared to healthy people; additionally, in people with ulcerative colitis, Proteobacteria and Actinobacteria appear to dominate; in people with Crohn's, <a href="/wiki/Enterococcus_faecium" title="Enterococcus faecium">Enterococcus faecium</a> and several Proteobacteria appear to be over-represented.<a href="#cite_note-Saxena2016-4">[4]</a> There is reasonable evidence that correcting gut flora imbalances by taking probiotics with <a href="/wiki/Lactobacilli" class="mw-redirect" title="Lactobacilli">Lactobacilli</a> and Bifidobacteria can reduce visceral pain and gut inflammation in IBD.<a href="#cite_note-JFP2016rev-131">[130]</a> <div class="mw-heading mw-heading3"><h3 id="Irritable_bowel_syndrome">Irritable bowel syndrome</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=39" title="Edit section: Irritable bowel syndrome">edit</a>]</div> <a href="/wiki/Irritable_bowel_syndrome" title="Irritable bowel syndrome">Irritable bowel syndrome</a> is a result of stress and chronic activation of the HPA axis; its symptoms include abdominal pain, changes in bowel movements, and an increase in proinflammatory cytokines. Overall, studies have found that the luminal and mucosal microbiota are changed in irritable bowel syndrome individuals, and these changes can relate to the type of irritation such as diarrhea or <a href="/wiki/Constipation" title="Constipation">constipation</a>. Also, there is a decrease in the diversity of the microbiome with low levels of fecal Lactobacilli and Bifidobacteria, high levels of facultative <a href="/wiki/Anaerobic_bacteria" class="mw-redirect" title="Anaerobic bacteria">anaerobic bacteria</a> such as <a href="/wiki/Escherichia_coli" title="Escherichia coli">Escherichia coli</a>, and increased ratios of Firmicutes: Bacteroidetes.<a href="#cite_note-DinanandCryan2015-125">[124]</a> <div class="mw-heading mw-heading4"><h4 id="Asthma">Asthma</h4>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=40" title="Edit section: Asthma">edit</a>]</div> With asthma, two hypotheses have been posed to explain its rising prevalence in the developed world. The <a href="/wiki/Hygiene_hypothesis" title="Hygiene hypothesis">hygiene hypothesis</a> posits that children in the developed world are not exposed to enough microbes and thus may contain lower prevalence of specific bacterial taxa that play protective roles.<a href="#cite_note-:2-156">[155]</a> The second hypothesis focuses on the <a href="/wiki/Western_pattern_diet" title="Western pattern diet">Western pattern diet</a>, which lacks <a href="/wiki/Whole_grain" title="Whole grain">whole grains</a> and <a href="/wiki/Dietary_fiber" title="Dietary fiber">fiber</a> and has an overabundance of <a href="/wiki/Simple_sugars" class="mw-redirect" title="Simple sugars">simple sugars</a>.<a href="#cite_note-Shen2016rev-15">[15]</a> Both hypotheses converge on the role of short-chain fatty acids (SCFAs) in <a href="/wiki/Immunotherapy" title="Immunotherapy">immunomodulation</a>. These bacterial fermentation metabolites are involved in immune signalling that prevents the triggering of asthma and lower SCFA levels are associated with the disease.<a href="#cite_note-:2-156">[155]</a><a href="#cite_note-:3-157">[156]</a> Lacking protective genera such as Lachnospira, <a href="/wiki/Veillonella" title="Veillonella">Veillonella</a>, <a href="/wiki/Rothia_(bacterium)" title="Rothia (bacterium)">Rothia</a> and <a href="/wiki/Faecalibacterium" title="Faecalibacterium">Faecalibacterium</a> has been linked to reduced SCFA levels.<a href="#cite_note-:2-156">[155]</a> Further, SCFAs are the product of bacterial fermentation of fiber, which is low in the Western pattern diet.<a href="#cite_note-Shen2016rev-15">[15]</a><a href="#cite_note-:3-157">[156]</a> SCFAs offer a link between gut flora and immune disorders, and as of 2016, this was an active area of research.<a href="#cite_note-Shen2016rev-15">[15]</a> Similar hypotheses have also been posited for the rise of food and other allergies.<a href="#cite_note-:02-158">[157]</a> <div class="mw-heading mw-heading4"><h4 id="Diabetes_mellitus_type_1">Diabetes mellitus type 1</h4>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=41" title="Edit section: Diabetes mellitus type 1">edit</a>]</div> The connection between the gut microbiota and <a href="/wiki/Diabetes_mellitus_type_1" class="mw-redirect" title="Diabetes mellitus type 1">diabetes mellitus type 1</a> has also been linked to SCFAs, such as <a href="/wiki/Butyrate" class="mw-redirect" title="Butyrate">butyrate</a> and acetate. Diets yielding butyrate and acetate from bacterial fermentation show increased <a href="/wiki/Regulatory_T_cell" title="Regulatory T cell">Treg</a> expression.<a href="#cite_note-159">[158]</a> <a href="/wiki/Regulatory_T_cell" title="Regulatory T cell">Treg</a> cells <a href="/wiki/Downregulation_and_upregulation" title="Downregulation and upregulation">downregulate</a> <a href="/wiki/T_cell" title="T cell">effector T cells</a>, which in turn reduces the <a href="/wiki/Inflammation" title="Inflammation">inflammatory response</a> in the gut.<a href="#cite_note-160">[159]</a> Butyrate is an energy source for colon cells. butyrate-yielding diets thus decrease <a href="/wiki/Intestinal_permeability" title="Intestinal permeability">gut permeability</a> by providing sufficient energy for the formation of <a href="/wiki/Tight_junction" title="Tight junction">tight junctions</a>.<a href="#cite_note-:4-161">[160]</a> Additionally, butyrate has also been shown to decrease insulin resistance, suggesting gut communities low in butyrate-producing microbes may increase chances of acquiring <a href="/wiki/Diabetes_mellitus_type_2" class="mw-redirect" title="Diabetes mellitus type 2">diabetes mellitus type 2</a>.<a href="#cite_note-:5-162">[161]</a> Butyrate-yielding diets may also have potential <a href="/wiki/Colorectal_cancer" title="Colorectal cancer">colorectal cancer</a> suppression effects.<a href="#cite_note-:4-161">[160]</a> <div class="mw-heading mw-heading3"><h3 id="Obesity_and_metabolic_syndrome">Obesity and metabolic syndrome</h3>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=42" title="Edit section: Obesity and metabolic syndrome">edit</a>]</div> The gut flora have been implicated in obesity and <a href="/wiki/Metabolic_syndrome" title="Metabolic syndrome">metabolic syndrome</a> due to a key role in the digestive process; the Western pattern diet appears to drive and maintain changes in the gut flora that in turn change how much energy is derived from food and how that energy is used.<a href="#cite_note-2016BoulangeRev-155">[154]</a><a href="#cite_note-163">[162]</a> One aspect of a <a href="/wiki/Healthy_diet" title="Healthy diet">healthy diet</a> that is often lacking in the <a href="/wiki/Western-pattern_diet" class="mw-redirect" title="Western-pattern diet">Western-pattern diet</a> is fiber and other complex carbohydrates that a healthy gut flora require flourishing; changes to gut flora in response to a Western-pattern diet appear to increase the amount of energy generated by the gut flora which may contribute to obesity and metabolic syndrome.<a href="#cite_note-JFP2016rev-131">[130]</a> There is also evidence that microbiota influence eating behaviours based on the preferences of the microbiota, which can lead to the host consuming more food eventually resulting in obesity. It has generally been observed that with higher gut microbiome diversity, the microbiota will spend energy and resources on competing with other microbiota and less on manipulating the host. The opposite is seen with lower gut microbiome diversity, and these microbiotas may work together to create host food cravings.<a href="#cite_note-Alcocketal2014-58">[58]</a> Additionally, the liver plays a dominant role in <a href="/wiki/Blood_glucose" class="mw-redirect" title="Blood glucose">blood glucose</a> homeostasis by maintaining a balance between the uptake and storage of glucose through the metabolic pathways of <a href="/wiki/Glycogenesis" title="Glycogenesis">glycogenesis</a> and <a href="/wiki/Gluconeogenesis" title="Gluconeogenesis">gluconeogenesis</a>. Intestinal lipids regulate glucose homeostasis involving a gut–brain–liver axis. The direct administration of lipids into the upper intestine increases the long chain fatty <a href="/wiki/Acyl-coenzyme_A" class="mw-redirect" title="Acyl-coenzyme A">acyl-coenzyme A</a> (LCFA-CoA) levels in the upper intestines and suppresses glucose production even under subdiaphragmatic <a href="/wiki/Vagotomy" title="Vagotomy">vagotomy</a> or gut vagal <a href="/wiki/Deafferentation" class="mw-redirect" title="Deafferentation">deafferentation</a>. This interrupts the neural connection between the brain and the gut and blocks the upper intestinal lipids' ability to inhibit glucose production. The gut–brain–liver axis and gut microbiota composition can regulate the glucose homeostasis in the liver and provide potential therapeutic methods to treat obesity and diabetes.<a href="#cite_note-Chen2013rev-164">[163]</a> Just as gut flora can function in a feedback loop that can drive the development of obesity, there is evidence that restricting intake of calories (i.e., <a href="/wiki/Dieting" title="Dieting">dieting</a>) can drive changes to the composition of the gut flora.<a href="#cite_note-2016BoulangeRev-155">[154]</a> <div class="mw-heading mw-heading2"><h2 id="Other_animals">Other animals</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=43" title="Edit section: Other animals">edit</a>]</div> The composition of the human gut microbiome is similar to that of the other great apes. However, humans' gut biota has decreased in diversity and changed in composition since our evolutionary split from Pan.<a href="#cite_note-ReferenceC-165">[164]</a> Humans display increases in Bacteroidetes, a bacterial phylum associated with diets high in animal protein and fat, and decreases in Methanobrevibacter and Fibrobacter, groups that ferment complex plant polysaccharides.<a href="#cite_note-ReferenceC-165">[164]</a> These changes are the result of the combined dietary, genetic, and cultural changes humans have undergone since evolutionary divergence from Pan.[<a href="/wiki/Wikipedia:Citation_needed" title="Wikipedia:Citation needed">citation needed</a>] In addition to humans and vertebrates, some insects also have complex and diverse gut microbiota that play key nutritional roles.<a href="#cite_note-Engel-2">[2]</a> Microbial communities associated with <a href="/wiki/Termite" title="Termite">termites</a> can constitute a majority of the weight of the individuals and perform important roles in the digestion of <a href="/wiki/Lignocellulose" class="mw-redirect" title="Lignocellulose">lignocellulose</a> and <a href="/wiki/Nitrogen_fixation" title="Nitrogen fixation">nitrogen fixation</a>.<a href="#cite_note-166">[165]</a> It is known that the disruption of gut microbiota of termites using agents like antibiotics<a href="#cite_note-167">[166]</a> or <a href="/wiki/Boric_acid" title="Boric acid">boric acid</a><a href="#cite_note-:1-168">[167]</a> (a common agent used in preventative treatment) causes severe damage to digestive function and leads to the rise of opportunistic pathogens.<a href="#cite_note-:1-168">[167]</a> These communities are host-specific, and closely related insect species share comparable similarities in gut microbiota composition.<a href="#cite_note-ReferenceA-169">[168]</a><a href="#cite_note-ReferenceB-170">[169]</a> In <a href="/wiki/Cockroach" title="Cockroach">cockroaches</a>, gut microbiota have been shown to assemble in a deterministic fashion, irrespective of the <a href="/wiki/Inoculation" title="Inoculation">inoculum</a>;<a href="#cite_note-171">[170]</a> the reason for this host-specific assembly remains unclear. Bacterial communities associated with insects like termites and cockroaches are determined by a combination of forces, primarily diet, but there is some indication that host <a href="/wiki/Phylogeny" class="mw-redirect" title="Phylogeny">phylogeny</a> may also be playing a role in the selection of lineages.<a href="#cite_note-ReferenceA-169">[168]</a><a href="#cite_note-ReferenceB-170">[169]</a> For more than 51 years it has been known that the administration of low doses of antibacterial agents promotes the growth of farm animals to increase weight gain.<a href="#cite_note-cho2012-130">[129]</a> In a study carried out on <a href="/wiki/Mice" class="mw-redirect" title="Mice">mice</a> the ratio of Firmicutes and <a href="/wiki/Lachnospiraceae" title="Lachnospiraceae">Lachnospiraceae</a> was significantly elevated in animals treated with subtherapeutic doses of different antibiotics. By analyzing the caloric content of faeces and the concentration of small chain fatty acids (SCFAs) in the GI tract, it was concluded that the changes in the composition of microbiota lead to an increased capacity to extract calories from otherwise indigestible constituents, and to an increased production of SCFAs. These findings provide evidence that antibiotics perturb not only the composition of the GI microbiome but also its metabolic capabilities, specifically with respect to SCFAs.<a href="#cite_note-cho2012-130">[129]</a> <div class="mw-heading mw-heading2"><h2 id="See_also">See also</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=44" title="Edit section: See also">edit</a>]</div> <style data-mw-deduplicate="TemplateStyles:r1239009302">.mw-parser-output .portalbox{padding:0;margin:0.5em 0;display:table;box-sizing:border-box;max-width:175px;list-style:none}.mw-parser-output .portalborder{border:1px solid var(--border-color-base,#a2a9b1);padding:0.1em;background:var(--background-color-neutral-subtle,#f8f9fa)}.mw-parser-output .portalbox-entry{display:table-row;font-size:85%;line-height:110%;height:1.9em;font-style:italic;font-weight:bold}.mw-parser-output .portalbox-image{display:table-cell;padding:0.2em;vertical-align:middle;text-align:center}.mw-parser-output .portalbox-link{display:table-cell;padding:0.2em 0.2em 0.2em 0.3em;vertical-align:middle}@media(min-width:720px){.mw-parser-output .portalleft{clear:left;float:left;margin:0.5em 1em 0.5em 0}.mw-parser-output .portalright{clear:right;float:right;margin:0.5em 0 0.5em 1em}}</style><ul role="navigation" aria-label="Portals" class="noprint portalbox portalborder portalright"> <li class="portalbox-entry"><a href="/wiki/File:Issoria_lathonia.jpg" class="mw-file-description"><img alt="icon" src="//upload.wikimedia.org/wikipedia/commons/thumb/2/2d/Issoria_lathonia.jpg/32px-Issoria_lathonia.jpg" decoding="async" width="32" height="23" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/2/2d/Issoria_lathonia.jpg/48px-Issoria_lathonia.jpg 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/2/2d/Issoria_lathonia.jpg/64px-Issoria_lathonia.jpg 2x" data-file-width="629" data-file-height="445" /></a><a href="/wiki/Portal:Biology" title="Portal:Biology">Biology portal</a></li><li class="portalbox-entry"><img alt="icon" src="//upload.wikimedia.org/wikipedia/commons/thumb/d/d6/WHO_Rod.svg/12px-WHO_Rod.svg.png" decoding="async" width="12" height="28" class="mw-file-element" srcset="//upload.wikimedia.org/wikipedia/commons/thumb/d/d6/WHO_Rod.svg/18px-WHO_Rod.svg.png 1.5x, //upload.wikimedia.org/wikipedia/commons/thumb/d/d6/WHO_Rod.svg/24px-WHO_Rod.svg.png 2x" data-file-width="107" data-file-height="250" /><a href="/wiki/Portal:Medicine" title="Portal:Medicine">Medicine portal</a></li></ul> <ul><li><a href="/wiki/Colonisation_resistance" class="mw-redirect" title="Colonisation resistance">Colonisation resistance</a></li> <li><a href="/wiki/List_of_human_flora" class="mw-redirect" title="List of human flora">List of human flora</a></li> <li><a href="/wiki/List_of_microbiota_species_of_the_lower_reproductive_tract_of_women" title="List of microbiota species of the lower reproductive tract of women">List of microbiota species of the lower reproductive tract of women</a></li> <li><a href="/wiki/Skin_flora" title="Skin flora">Skin flora</a></li> <li><a href="/wiki/Verotoxin-producing_Escherichia_coli" class="mw-redirect" title="Verotoxin-producing Escherichia coli">Verotoxin-producing Escherichia coli</a></li></ul> <div class="mw-heading mw-heading2"><h2 id="Notes">Notes</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=45" title="Edit section: Notes">edit</a>]</div> <style data-mw-deduplicate="TemplateStyles:r1239543626">.mw-parser-output .reflist{margin-bottom:0.5em;list-style-type:decimal}@media screen{.mw-parser-output .reflist{font-size:90%}}.mw-parser-output .reflist .references{font-size:100%;margin-bottom:0;list-style-type:inherit}.mw-parser-output .reflist-columns-2{column-width:30em}.mw-parser-output .reflist-columns-3{column-width:25em}.mw-parser-output .reflist-columns{margin-top:0.3em}.mw-parser-output .reflist-columns ol{margin-top:0}.mw-parser-output .reflist-columns li{page-break-inside:avoid;break-inside:avoid-column}.mw-parser-output .reflist-upper-alpha{list-style-type:upper-alpha}.mw-parser-output .reflist-upper-roman{list-style-type:upper-roman}.mw-parser-output .reflist-lower-alpha{list-style-type:lower-alpha}.mw-parser-output .reflist-lower-greek{list-style-type:lower-greek}.mw-parser-output .reflist-lower-roman{list-style-type:lower-roman}</style><div class="reflist"> <div class="mw-references-wrap"><ol class="references"> <li id="cite_note-96"><a href="#cite_ref-96">^</a> There is substantial variation in microbiome composition and microbial concentrations by anatomical site.<a href="#cite_note-Pharmacomicrobiomics-94">[94]</a><a href="#cite_note-Human_microbiome-95">[95]</a> Fluid from the human colon – which contains the highest concentration of microbes of any anatomical site – contains approximately one trillion (10^12) bacterial cells/ml.<a href="#cite_note-Pharmacomicrobiomics-94">[94]</a> </li> </ol></div></div> <div class="mw-heading mw-heading2"><h2 id="References">References</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=46" title="Edit section: References">edit</a>]</div> <link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1239543626"><div class="reflist reflist-columns references-column-width" style="column-width: 30em;"> <ol class="references"> <li id="cite_note-Moszak-1"><a href="#cite_ref-Moszak_1-0">^</a> <style data-mw-deduplicate="TemplateStyles:r1238218222">.mw-parser-output cite.citation{font-style:inherit;word-wrap:break-word}.mw-parser-output .citation q{quotes:"\"""\"""'""'"}.mw-parser-output .citation:target{background-color:rgba(0,127,255,0.133)}.mw-parser-output .id-lock-free.id-lock-free a{background:url("//upload.wikimedia.org/wikipedia/commons/6/65/Lock-green.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-limited.id-lock-limited a,.mw-parser-output .id-lock-registration.id-lock-registration a{background:url("//upload.wikimedia.org/wikipedia/commons/d/d6/Lock-gray-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-subscription.id-lock-subscription a{background:url("//upload.wikimedia.org/wikipedia/commons/a/aa/Lock-red-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .cs1-ws-icon a{background:url("//upload.wikimedia.org/wikipedia/commons/4/4c/Wikisource-logo.svg")right 0.1em center/12px no-repeat}body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .id-lock-free a,body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .id-lock-limited a,body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .id-lock-registration a,body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .id-lock-subscription a,body:not(.skin-timeless):not(.skin-minerva) .mw-parser-output .cs1-ws-icon a{background-size:contain;padding:0 1em 0 0}.mw-parser-output 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Applied and Environmental Microbiology. 82 (4): 1256–1263. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1128%2FAEM.03700-15">10.1128/AEM.03700-15</a>. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751828">4751828</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/26655763">26655763</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Applied+and+Environmental+Microbiology&rft.atitle=The+deterministic+assembly+of+complex+bacterial+communities+in+germ-free+cockroach+guts&rft.volume=82&rft.issue=4&rft.pages=1256-1263&rft.date=2016&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC4751828%23id-name%3DPMC&rft_id=info%3Apmid%2F26655763&rft_id=info%3Adoi%2F10.1128%2FAEM.03700-15&rft.aulast=Mikaelyan&rft.aufirst=A.&rft.au=Thompson%2C+C.&rft.au=Hofer%2C+M.&rft.au=Brune%2C+A.&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC4751828&rfr_id=info%3Asid%2Fen.wikipedia.org%3AGut+microbiota" class="Z3988"> </li> </ol></div> <div class="mw-heading mw-heading2"><h2 id="Further_reading">Further reading</h2>[<a href="/w/index.php?title=Gut_microbiota&action=edit&section=47" title="Edit section: Further reading">edit</a>]</div> <dl><dt>Review articles</dt></dl> <ul><li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFDe_PreterHamerWindeyVerbeke2011" class="citation journal cs1">De Preter, Vicky; Hamer, Henrike M; Windey, Karen; Verbeke, Kristin (2011). "The impact of pre- and/or probiotics on human colonic metabolism: Does it affect human health?". Molecular Nutrition & Food Research. 55 (1): 46–57. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1002%2Fmnfr.201000451">10.1002/mnfr.201000451</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/21207512">21207512</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Molecular+Nutrition+%26+Food+Research&rft.atitle=The+impact+of+pre-+and%2For+probiotics+on+human+colonic+metabolism%3A+Does+it+affect+human+health%3F&rft.volume=55&rft.issue=1&rft.pages=46-57&rft.date=2011&rft_id=info%3Adoi%2F10.1002%2Fmnfr.201000451&rft_id=info%3Apmid%2F21207512&rft.aulast=De+Preter&rft.aufirst=Vicky&rft.au=Hamer%2C+Henrike+M&rft.au=Windey%2C+Karen&rft.au=Verbeke%2C+Kristin&rfr_id=info%3Asid%2Fen.wikipedia.org%3AGut+microbiota" class="Z3988"></li> <li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFMarandubaDe_CastroSouzaRossato2015" class="citation journal cs1">Maranduba, Carlos Magno da Costa; De Castro, Sandra Bertelli Ribeiro; Souza, Gustavo Torres de; Rossato, Cristiano; Da Guia, Francisco Carlos; Valente, Maria Anete Santana; Rettore, João Vitor Paes; Maranduba, Claudinéia Pereira; Souza, Camila Maurmann de; Carmo, Antônio Márcio Resende do; MacEdo, Gilson Costa; Silva, Fernando de Sá (2015). <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352473">"Intestinal Microbiota as Modulators of the Immune System and Neuroimmune System: Impact on the Host Health and Homeostasis"</a>. Journal of Immunology Research. 2015: 931574. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1155%2F2015%2F931574">10.1155/2015/931574</a>. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352473">4352473</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/25759850">25759850</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Journal+of+Immunology+Research&rft.atitle=Intestinal+Microbiota+as+Modulators+of+the+Immune+System+and+Neuroimmune+System%3A+Impact+on+the+Host+Health+and+Homeostasis&rft.volume=2015&rft.pages=931574&rft.date=2015&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC4352473%23id-name%3DPMC&rft_id=info%3Apmid%2F25759850&rft_id=info%3Adoi%2F10.1155%2F2015%2F931574&rft.aulast=Maranduba&rft.aufirst=Carlos+Magno+da+Costa&rft.au=De+Castro%2C+Sandra+Bertelli+Ribeiro&rft.au=Souza%2C+Gustavo+Torres+de&rft.au=Rossato%2C+Cristiano&rft.au=Da+Guia%2C+Francisco+Carlos&rft.au=Valente%2C+Maria+Anete+Santana&rft.au=Rettore%2C+Jo%C3%A3o+Vitor+Paes&rft.au=Maranduba%2C+Claudin%C3%A9ia+Pereira&rft.au=Souza%2C+Camila+Maurmann+de&rft.au=Carmo%2C+Ant%C3%B4nio+M%C3%A1rcio+Resende+do&rft.au=MacEdo%2C+Gilson+Costa&rft.au=Silva%2C+Fernando+de+S%C3%A1&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC4352473&rfr_id=info%3Asid%2Fen.wikipedia.org%3AGut+microbiota" class="Z3988"></li> <li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFPrakashRodesCoussa-CharleyTomaro-Duchesneau2011" class="citation journal cs1">Prakash, Satya; Rodes, Laetitia; Coussa-Charley, Michael; Tomaro-Duchesneau, Catherine; Tomaro-Duchesneau, Catherine; Coussa-Charley; Rodes (2011). <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156250">"Gut microbiota: Next frontier in understanding human health and development of biotherapeutics"</a>. Biologics: Targets and Therapy. 5: 71–86. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.2147%2FBTT.S19099">10.2147/BTT.S19099</a>. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156250">3156250</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/21847343">21847343</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Biologics%3A+Targets+and+Therapy&rft.atitle=Gut+microbiota%3A+Next+frontier+in+understanding+human+health+and+development+of+biotherapeutics&rft.volume=5&rft.pages=71-86&rft.date=2011&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3156250%23id-name%3DPMC&rft_id=info%3Apmid%2F21847343&rft_id=info%3Adoi%2F10.2147%2FBTT.S19099&rft.aulast=Prakash&rft.aufirst=Satya&rft.au=Rodes%2C+Laetitia&rft.au=Coussa-Charley%2C+Michael&rft.au=Tomaro-Duchesneau%2C+Catherine&rft.au=Tomaro-Duchesneau%2C+Catherine&rft.au=Coussa-Charley&rft.au=Rodes&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3156250&rfr_id=info%3Asid%2Fen.wikipedia.org%3AGut+microbiota" class="Z3988"></li> <li><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1238218222"><cite id="CITEREFWuChenHoffmannBittinger2011" class="citation journal cs1">Wu, G. D.; Chen, J.; Hoffmann, C.; Bittinger, K.; Chen, Y.-Y.; Keilbaugh, S. A.; Bewtra, M.; Knights, D.; Walters, W. A.; Knight, R.; Sinha, R.; Gilroy, E.; Gupta, K.; Baldassano, R.; Nessel, L.; Li, H.; Bushman, F. D.; Lewis, J.D. (2011). <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368382">"Linking Long-Term Dietary Patterns with Gut Microbial Enterotypes"</a>. Science. 334 (6052): 105–108. <a href="/wiki/Bibcode_(identifier)" class="mw-redirect" title="Bibcode (identifier)">Bibcode</a>:<a rel="nofollow" class="external text" href="https://ui.adsabs.harvard.edu/abs/2011Sci...334..105W">2011Sci...334..105W</a>. <a href="/wiki/Doi_(identifier)" class="mw-redirect" title="Doi (identifier)">doi</a>:<a rel="nofollow" class="external text" href="https://doi.org/10.1126%2Fscience.1208344">10.1126/science.1208344</a>. <a href="/wiki/PMC_(identifier)" class="mw-redirect" title="PMC (identifier)">PMC</a> <a rel="nofollow" class="external text" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3368382">3368382</a>. <a href="/wiki/PMID_(identifier)" class="mw-redirect" title="PMID (identifier)">PMID</a> <a rel="nofollow" class="external text" href="https://pubmed.ncbi.nlm.nih.gov/21885731">21885731</a>.</cite><span title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.jtitle=Science&rft.atitle=Linking+Long-Term+Dietary+Patterns+with+Gut+Microbial+Enterotypes&rft.volume=334&rft.issue=6052&rft.pages=105-108&rft.date=2011&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3368382%23id-name%3DPMC&rft_id=info%3Apmid%2F21885731&rft_id=info%3Adoi%2F10.1126%2Fscience.1208344&rft_id=info%3Abibcode%2F2011Sci...334..105W&rft.aulast=Wu&rft.aufirst=G.+D.&rft.au=Chen%2C+J.&rft.au=Hoffmann%2C+C.&rft.au=Bittinger%2C+K.&rft.au=Chen%2C+Y.-Y.&rft.au=Keilbaugh%2C+S.+A.&rft.au=Bewtra%2C+M.&rft.au=Knights%2C+D.&rft.au=Walters%2C+W.+A.&rft.au=Knight%2C+R.&rft.au=Sinha%2C+R.&rft.au=Gilroy%2C+E.&rft.au=Gupta%2C+K.&rft.au=Baldassano%2C+R.&rft.au=Nessel%2C+L.&rft.au=Li%2C+H.&rft.au=Bushman%2C+F.+D.&rft.au=Lewis%2C+J.D.&rft_id=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC3368382&rfr_id=info%3Asid%2Fen.wikipedia.org%3AGut+microbiota" class="Z3988"></li></ul> <div class="navbox-styles"><link rel="mw-deduplicated-inline-style" href="mw-data:TemplateStyles:r1129693374"><style data-mw-deduplicate="TemplateStyles:r1236075235">.mw-parser-output .navbox{box-sizing:border-box;border:1px solid #a2a9b1;width:100%;clear:both;font-size:88%;text-align:center;padding:1px;margin:1em auto 0}.mw-parser-output .navbox .navbox{margin-top:0}.mw-parser-output .navbox+.navbox,.mw-parser-output .navbox+.navbox-styles+.navbox{margin-top:-1px}.mw-parser-output .navbox-inner,.mw-parser-output .navbox-subgroup{width:100%}.mw-parser-output .navbox-group,.mw-parser-output .navbox-title,.mw-parser-output .navbox-abovebelow{padding:0.25em 1em;line-height:1.5em;text-align:center}.mw-parser-output .navbox-group{white-space:nowrap;text-align:right}.mw-parser-output .navbox,.mw-parser-output .navbox-subgroup{background-color:#fdfdfd}.mw-parser-output .navbox-list{line-height:1.5em;border-color:#fdfdfd}.mw-parser-output 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