{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T04:22:42Z","timestamp":1788495762419,"version":"build-2803163510"},"reference-count":46,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2020,7,28]],"date-time":"2020-07-28T00:00:00Z","timestamp":1595894400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Chongqing Health and Family Planning Commission","award":["ZY201802022"],"award-info":[{"award-number":["ZY201802022"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2020,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Mechanistic target of rapamycin complex 1 (mTORC1) functions as regulating different cellular processes, including cell growth, proliferation, motility, survival, metabolism, autophagy, and protein transcription. Recently, it also found to be associated with many infections and inflammatory diseases, playing complex roles in pathogens growth and inflammation regulation. However, the regulation mechanism of mTORC1 in gastric epithelial cells and its role in <jats:italic>Helicobacter pylori (H. pylori)<\/jats:italic> infection and related gastritis remain unclear. Here, we identified that the phosphorylation of mechanistic target of rapamycin (mTOR) and the expression of DEP domain\u2010containing mTOR\u2010interacting protein (DEPTOR) was increased in gastric mucosa of <jats:italic>H. pylori<\/jats:italic>\u2010infected patients and mice, as well as in <jats:italic>H. pylori<\/jats:italic>\u2010infected gastric epithelial cells, which were largely depended on <jats:italic>H. pylori cagA<\/jats:italic>. The expression of DEPTOR was regulated via mTORC1, but, in turn, inhibited mTORC1. Knockdown mTOR significantly decreased expression and secretion of cytokines tumor necrosis factor\u2010\u03b1, interleukin\u20101\u03b2, and interleukin\u20106, chemokines CCL7 and CXCL16, and antimicrobial peptide LL37 in vitro, while knockdown DEPTOR had the opposite effect. Similar observations were made using mTOR knockout (KO) mice in vivo, moreover. The gastric inflammation was attenuated, while the bacterial burden was increased in mTOR KO mice during <jats:italic>H. pylori<\/jats:italic> infection. These findings supported <jats:italic>H. pylori<\/jats:italic> promote gastritis and inhibit bacterial colonization through the <jats:italic>cagA<\/jats:italic>\u2010dependent activation of mTORC1.<\/jats:p>","DOI":"10.1002\/jcp.29826","type":"journal-article","created":{"date-parts":[[2020,7,28]],"date-time":"2020-07-28T23:57:10Z","timestamp":1595980630000},"page":"10094-10108","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["<i>Helicobacter pylori<\/i> promote inflammation and host defense through the <i>cagA<\/i>\u2010dependent activation of mTORC1"],"prefix":"10.1002","volume":"235","author":[{"given":"Guang\u2010Jing","family":"Feng","sequence":"first","affiliation":[{"name":"Department of General Surgery Chongqing Traditional Chinese Medicine Hospital  Chongqing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Chen","sequence":"additional","affiliation":[{"name":"Department 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