Helicobacter pylori cagA + Strains and Dissociation of Gastric Epithelial Cell Proliferation From Apoptosis | JNCI: Journal of the National Cancer Institute

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Background: Infection with Helicobacter pylori induces chronic gastritis in virtually all infected persons, and such gastritis has been associate","pageStart":"863","pageEnd":"868","siteName":"OUP Academic","thumbnailURL":"https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/jnci/89/12/10.1093_jnci_89.12.863/2/m_89-12-863-fig001.jpeg?Expires=1794517225&Signature=L4~BXIUlOnTe5AiV~Is9b7C2MUbZ9wHQQBNItccnN-ACP4dzJxIUbUpl8~KJXxNrTkb3iOX7ccXfLbSNJR7xfJNds~9tAzbDCK-W~0WE5iqC300swf3Oo0Y0JLKSCYMSwAsTtJmUhLZCPoZrlunByHaQt1wiS7~uvQ7mJI0zTUm1BWHWWWar1wjZq63L9c8eaTj3cZw1oWYTsIKaMJsc5bGYILnhq5iwZXOzEFYwfAgCzKSNElzp5uGSGzd0g0HzXA616tJJLpBe1uJRIC6mEnI4A5DpDlTmsgT2wPCkMN~TTsPFHxIFoRUUFEvLE9cZfheli-UZ5CSwMuG0ZDCghg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA","headline":"Helicobacter pylori cagA + Strains and Dissociation of Gastric Epithelial Cell Proliferation From Apoptosis","image":"https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/jnci/89/12/10.1093_jnci_89.12.863/2/m_89-12-863-fig001.jpeg?Expires=1794517225&Signature=L4~BXIUlOnTe5AiV~Is9b7C2MUbZ9wHQQBNItccnN-ACP4dzJxIUbUpl8~KJXxNrTkb3iOX7ccXfLbSNJR7xfJNds~9tAzbDCK-W~0WE5iqC300swf3Oo0Y0JLKSCYMSwAsTtJmUhLZCPoZrlunByHaQt1wiS7~uvQ7mJI0zTUm1BWHWWWar1wjZq63L9c8eaTj3cZw1oWYTsIKaMJsc5bGYILnhq5iwZXOzEFYwfAgCzKSNElzp5uGSGzd0g0HzXA616tJJLpBe1uJRIC6mEnI4A5DpDlTmsgT2wPCkMN~TTsPFHxIFoRUUFEvLE9cZfheli-UZ5CSwMuG0ZDCghg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA","image:alt":"Proliferation scores ( A ) are higher but apoptosis scores ( B ) and apoptosis/proliferation ratios ( C ) are lower in the gastric antrum in persons infected with cagA +Helicobacter pylori strains. Epithelial cell proliferation was scored 1-3 by use of immunoperoxidase staining with Mib-1 anti-Ki-67 antibody by a single pathologist blinded to H. pylori genotype. Apoptosis was quantitated by use of the terminal uridine deoxynucleotidyl nick end-labeling (TUNEL) assay and expressed as apoptotic cellular index (number of positively stained epithelial cells/100 epithelial cells counted). The apoptosis/ proliferation ratio was determined by dividing the apoptotic cellular index by the proliferation score. cagA status of infecting isolates was determined by the serology and polymerase chain reaction of genomic DNA. Each data point reflects averaged scores from two antral biopsy specimens (one data point per patient). Median values with interquartile ranges are shown adjacent to data points."} </script> <meta property="og:site_name" content="OUP Academic" /> <meta property="og:title" content="Helicobacter pylori cagA + Strains and Dissociation of Gastric Epithelial Cell Proliferation From Apoptosis" /> <meta property="og:description" content="Abstract. Background: Infection with Helicobacter pylori induces chronic gastritis in virtually all infected persons, and such gastritis has been associate" /> <meta property="og:type" content="article" /> <meta property="og:url" content="https://dx.doi.org/10.1093/jnci/89.12.863" /> <meta property="og:updated_time" content="" /> <meta property="og:image" content="https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/jnci/89/12/10.1093_jnci_89.12.863/2/m_89-12-863-fig001.jpeg?Expires=1794517225&Signature=L4~BXIUlOnTe5AiV~Is9b7C2MUbZ9wHQQBNItccnN-ACP4dzJxIUbUpl8~KJXxNrTkb3iOX7ccXfLbSNJR7xfJNds~9tAzbDCK-W~0WE5iqC300swf3Oo0Y0JLKSCYMSwAsTtJmUhLZCPoZrlunByHaQt1wiS7~uvQ7mJI0zTUm1BWHWWWar1wjZq63L9c8eaTj3cZw1oWYTsIKaMJsc5bGYILnhq5iwZXOzEFYwfAgCzKSNElzp5uGSGzd0g0HzXA616tJJLpBe1uJRIC6mEnI4A5DpDlTmsgT2wPCkMN~TTsPFHxIFoRUUFEvLE9cZfheli-UZ5CSwMuG0ZDCghg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA" /> <meta property="og:image:url" content="https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/jnci/89/12/10.1093_jnci_89.12.863/2/m_89-12-863-fig001.jpeg?Expires=1794517225&Signature=L4~BXIUlOnTe5AiV~Is9b7C2MUbZ9wHQQBNItccnN-ACP4dzJxIUbUpl8~KJXxNrTkb3iOX7ccXfLbSNJR7xfJNds~9tAzbDCK-W~0WE5iqC300swf3Oo0Y0JLKSCYMSwAsTtJmUhLZCPoZrlunByHaQt1wiS7~uvQ7mJI0zTUm1BWHWWWar1wjZq63L9c8eaTj3cZw1oWYTsIKaMJsc5bGYILnhq5iwZXOzEFYwfAgCzKSNElzp5uGSGzd0g0HzXA616tJJLpBe1uJRIC6mEnI4A5DpDlTmsgT2wPCkMN~TTsPFHxIFoRUUFEvLE9cZfheli-UZ5CSwMuG0ZDCghg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA" /> <meta property="og:image:secure_url" content="https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/jnci/89/12/10.1093_jnci_89.12.863/2/m_89-12-863-fig001.jpeg?Expires=1794517225&Signature=L4~BXIUlOnTe5AiV~Is9b7C2MUbZ9wHQQBNItccnN-ACP4dzJxIUbUpl8~KJXxNrTkb3iOX7ccXfLbSNJR7xfJNds~9tAzbDCK-W~0WE5iqC300swf3Oo0Y0JLKSCYMSwAsTtJmUhLZCPoZrlunByHaQt1wiS7~uvQ7mJI0zTUm1BWHWWWar1wjZq63L9c8eaTj3cZw1oWYTsIKaMJsc5bGYILnhq5iwZXOzEFYwfAgCzKSNElzp5uGSGzd0g0HzXA616tJJLpBe1uJRIC6mEnI4A5DpDlTmsgT2wPCkMN~TTsPFHxIFoRUUFEvLE9cZfheli-UZ5CSwMuG0ZDCghg__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA" /> <meta property="og:image:alt" content="Proliferation scores ( A ) are higher but apoptosis scores ( B ) and apoptosis/proliferation ratios ( C ) are lower in the gastric antrum in persons infected with cagA +Helicobacter pylori strains. Epithelial cell proliferation was scored 1-3 by use of immunoperoxidase staining with Mib-1 anti-Ki-67 antibody by a single pathologist blinded to H. pylori genotype. Apoptosis was quantitated by use of the terminal uridine deoxynucleotidyl nick end-labeling (TUNEL) assay and expressed as apoptotic cellular index (number of positively stained epithelial cells/100 epithelial cells counted). The apoptosis/ proliferation ratio was determined by dividing the apoptotic cellular index by the proliferation score. cagA status of infecting isolates was determined by the serology and polymerase chain reaction of genomic DNA. Each data point reflects averaged scores from two antral biopsy specimens (one data point per patient). Median values with interquartile ranges are shown adjacent to data points." /> <meta name="twitter:card" content="summary_large_image" /> <meta name="citation_author" content="Peek, Richard M." /><meta name="citation_author_institution" content="Division of Gastroenterology, Department of Medicine, Vanderbilt University School of Medicine, and Department of Veterans Affairs Medical Center , Nashville, TN" /><meta name="citation_author" content="Moss, Steven F." /><meta name="citation_author_institution" content="Division of Gastroenterology, Department of Medicine, St. Luke's-Roosevelt Hospital Center, Columbia University , New York" /><meta name="citation_author" content="Wang, Shaobai" /><meta name="citation_author_institution" content="Division of Gastroenterology, Department of Medicine, St. Luke's-Roosevelt Hospital Center, Columbia University , New York" /><meta name="citation_author" content="Holt, Peter R." /><meta name="citation_author_institution" content="Division of Gastroenterology, Department of Medicine, St. Luke's-Roosevelt Hospital Center, Columbia University , New York" /><meta name="citation_author" content="Tham, Kyi T." /><meta name="citation_author_institution" content="Department of Veterans Affairs Medical Center , Nashville" /><meta name="citation_author_institution" content="Department of Pathology, Vanderbilt University School of Mediciney" /><meta name="citation_author" content="Blaser, Martin J." /><meta name="citation_author_institution" content="Department of Veterans Affairs Medical Center , Nashville" /><meta name="citation_author_institution" content="Division of Infectious Diseases, Department of Medicine, Vanderbilt University School of Medicine" /><meta name="citation_author" content="Pérez-Pérez, Guillermo I." /><meta name="citation_author_institution" content="Division of Infectious Diseases, Department of Medicine, Vanderbilt University School of Medicine" /><meta name="citation_author" content="Miller, Geraldine G." /><meta name="citation_author_institution" content="Division of Infectious Diseases, Department of Medicine, Vanderbilt University School of Medicine" /><meta name="citation_author" content="Atherton, John C." /><meta name="citation_author_institution" content="Division of Infectious Diseases, Department of Medicine, Vanderbilt University School of Medicine" /><meta name="citation_title" content="Helicobacter pylori cagA + Strains and Dissociation of Gastric Epithelial Cell Proliferation From Apoptosis " /><meta name="citation_firstpage" content="863" /><meta name="citation_lastpage" content="868" /><meta name="citation_doi" content="10.1093/jnci/89.12.863" /><meta name="citation_keyword" content="apoptosis" /><meta name="citation_keyword" content="helicobacter pylori" /><meta name="citation_keyword" content="epithelial cells" /><meta name="citation_keyword" content="cytotoxin-associated gene a" /><meta name="citation_keyword" content="infections" /><meta name="citation_keyword" content="inflammation" /><meta name="citation_keyword" content="genotype" /><meta name="citation_journal_title" content="JNCI: Journal of the National Cancer Institute" /><meta name="citation_journal_abbrev" content="J Natl Cancer Inst" /><meta name="citation_volume" content="89" /><meta name="citation_issue" content="12" /><meta name="citation_publication_date" content="1997/06/18" /><meta name="citation_issn" content="0027-8874" /><meta name="citation_publisher" content="Oxford Academic" /><meta name="citation_reference" content="citation_title=Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric pH; 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This risk is further enhanced with cagA <sup>+</sup> (positive for cytotoxin-associated gene A) <em>H. pylori</em> strains and may be a consequence of induced gastric cell proliferation and/or alteration in apoptosis (programmed cell death) in the gastric epithelium. <em>Purpose:</em> To determine whether the <em>H. pylori</em> cagA genotype and another virulence-related characteristic, the vacA (vacuolating cytotoxin A) s1a genotype, differentially affect epithelial cell proliferation, apoptosis, and the histologic parameters of inflammation and injury, we quantitated these characteristics in infected and uninfected persons. <em>Methods:</em> Fifty patients underwent upper gastrointestinal endoscopy, and biopsy specimens were taken. Apoptotic cells in the specimens were quantitated after terminal deoxynucleotidyl transferase labeling of DNA fragments with digoxigenin-deoxyuridine triphosphate; epithelial cell proliferation was scored by immunohistochemical analysis of the proliferation-associated antigen Ki-67. Antibodies directed against <em>H. pylori</em> and CagA protein were measured in the serum of patients by means of enzyme- linked immunosorbent assays. Analysis of <em>H. pylori</em> genomic DNA, by use of the polymerase chain reaction, was performed to determine the cagA and vacA genotypes. Acute and chronic inflammation, epithelial cell degeneration, mucin depletion, intestinal metaplasia, glandular atrophy, and vacuolation were each scored in a blinded manner. Reported <em>P</em> values are twosided. <em>Results:</em> Persons harboring cagA <sup>+</sup> strains (n = 20) had significantly higher gastric epithelial proliferation scores than persons infected with cagA <sup>−</sup> strains (n = 9) or uninfected persons (n = 21) ( <em>P</em> = .025 and P<.001, respectively), but the difference in cell proliferation between the latter two groups was not statistically significant. The number of apoptotic cells per 100 epithelial cells (apoptotic index) in persons infected with cagA <sup>+</sup> strains was lower than in persons infected with cagA- strains ( <em>P</em> = .05). Apoptotic indices in the cagA <sup>+</sup> group were similar to those in the uninfected group ( <em>P</em> = .2). Epithelial cell proliferation was significantly correlated with acute gastric inflammation, but only in the cagA <sup>+</sup> group ( <em>r</em> = .44; <em>P</em> = .006). The cagA <sup>+</sup> and vacA s1a genotypes were found to be concordant, confirming the close relationship between these virulencerelated genotypes. <em>Conclusions:</em> Gastric mucosal proliferation was significantly correlated with the severity of acute gastritis in persons infected with cagA <sup>+</sup> vacA s1a strains of <em>H. pylori</em> . This increased proliferation was not accompanied by a parallel increase in apoptosis. <em>Implications:</em> Increased cell proliferation in the absence of a corresponding increase in apoptosis may explain the heightened risk for gastric carcinoma that is associated with infection by cagA <sup>+</sup> vacA s1a strains of <em>H. pylori</em> . </p></section> <div class="article-metadata-panel clearfix at-ArticleMetadata"></div>  <div class="widget widget-ArticlePubStateInfo widget-instance-OUP_ArticlePubStateInfo"> </div> <div class="article-metadata-standalone-panel clearfix"></div> <div class="copyright copyright-statement">© Oxford University Press</div> <span id="UserHasAccess" data-userHasAccess="False"></span> </div> </div> </div> <div class="widget widget-RelatedTags widget-instance-OUP_Article_RelatedTags_Widget"> <div class="related-topic-tags"> <div class="related-topic-tag-label">Topic:</div> <ul class="related-topic-tag-list"> <li> <a class="js-qb-topic-keyword-search" 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Helicobacter pylori cagA + Strains and Dissociation of Gastric Epithelial Cell Proliferation From Apoptosis | JNCI: Journal of the National Cancer Institute | Oxford Academic