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Loss of parietal cells causes the development of <jats:styled-content style=\"fixed-case\">SPEM<\/jats:styled-content> in the gastric corpus and then chronic inflammation drives <jats:styled-content style=\"fixed-case\">SPEM<\/jats:styled-content> toward a more proliferative lineage. Mongolian gerbils infected with <jats:italic>Helicobacter pylori<\/jats:italic> develop chronic gastritis and metaplasia, mimicking aspects of human gastritis with <jats:italic>H. pylori<\/jats:italic> infection. We therefore examined metaplastic lineages in the gastric corpus mucosa of gerbils infected by <jats:italic>H. pylori<\/jats:italic> strain 7.13, which produces rapid onset of severe inflammation. Six weeks following <jats:italic>H. pylori<\/jats:italic> infection, <jats:italic>Griffonia simplicifolia<\/jats:italic> lectin <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">GSII<\/jats:styled-content>)\u2010positive <jats:styled-content style=\"fixed-case\">SPEM<\/jats:styled-content> developed in the base of oxyntic glands in association with parietal cell loss and inflammation. In association with severe inflammation, <jats:styled-content style=\"fixed-case\">SPEM<\/jats:styled-content> glands evolved into aberrant phenotypes, including branched lesions, dilated lesions, and penetrating invasive glands. Mucin 4 (<jats:styled-content style=\"fixed-case\">MUC4<\/jats:styled-content>) was up\u2010regulated in <jats:styled-content style=\"fixed-case\">SPEM<\/jats:styled-content> and progressive <jats:styled-content style=\"fixed-case\">SPEM<\/jats:styled-content>. Clusterin was expressed in the tips of branched and dilated lesions and throughout regions of invasive glands. Intriguingly, clusterin\u2010positive regions in these lesions expressed Ki67 and matrix metalloproteinase 7 (<jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>\u20107). These same regions were also positive for expression of phospho\u2010<jats:styled-content style=\"fixed-case\">IkB\u03b1<\/jats:styled-content>, suggestive of activated <jats:styled-content style=\"fixed-case\">NFkB<\/jats:styled-content> signalling. These findings suggest that clusterin\u2010positive regions in progressive phenotypes of <jats:styled-content style=\"fixed-case\">SPEM<\/jats:styled-content> have invasive characteristics. Thus, <jats:italic>H. pylori<\/jats:italic> infection in gerbils induces <jats:styled-content style=\"fixed-case\">SPEM<\/jats:styled-content>, which then can progress to further aberrant and invasive metaplastic phenotypes. Copyright \u00a9 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/path.4735","type":"journal-article","created":{"date-parts":[[2016,4,30]],"date-time":"2016-04-30T09:26:50Z","timestamp":1462008410000},"page":"399-410","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["Characterization of progressive metaplasia in the gastric corpus mucosa of Mongolian gerbils infected with <i>Helicobacter pylori<\/i>"],"prefix":"10.1002","volume":"239","author":[{"given":"Takahiro","family":"Shimizu","sequence":"first","affiliation":[{"name":"Nashville VA Medical Center  Nashville Tennessee USA"},{"name":"Departments of Surgery and Cell and Developmental Biology and the Epithelial Biology Center Vanderbilt University School of Medicine  Nashville Tennessee USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eunyoung","family":"Choi","sequence":"additional","affiliation":[{"name":"Nashville VA Medical Center  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