{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T17:16:27Z","timestamp":1768583787373,"version":"3.49.0"},"reference-count":43,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2020,7,26]],"date-time":"2020-07-26T00:00:00Z","timestamp":1595721600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Persistent <jats:italic>Helicobacter pylori<\/jats:italic> infection induces gastric mucosal atrophy, which is a precancerous condition. Hydrogen sulfide (H<jats:sub>2<\/jats:sub>S), a gaseous biological transmitter, has been implicated in both the physiological functions of the gastrointestinal tract and its diseases. To understand gastric epithelial cell response against <jats:italic>H\u00a0pylori<\/jats:italic> infection, we investigated the metabolic changes of gastric cancer cells co\u2010cultured with <jats:italic>H\u00a0pylori<\/jats:italic> and observed the modulation of endogenous H<jats:sub>2<\/jats:sub>S production.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>Gastric cancer AGS cells were co\u2010cultured with an <jats:italic>H\u00a0pylori<\/jats:italic> standard strain possessing bacterial virulence factor CagA (ATCC 43504) and a strain without CagA (ATCC 51932). Three hours after inoculation, the cells were subjected to metabolomics analysis using gas chromatography\u2010tandem mass spectrometry (GC\u2010MS\/MS). Orthogonal projections to latent structures discriminant analysis (OPLS\u2010DA) and pathway analysis were performed. In addition, intracellular H<jats:sub>2<\/jats:sub>S levels were measured by using HSip\u20101 fluorescent probe.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Results of OPLS\u2010DA showed a significant difference between the metabolism of untreated control cells and cells inoculated with the <jats:italic>H\u00a0pylori<\/jats:italic> strains ATCC 51932 or ATCC 43504, mainly due to 45 metabolites. Pathway analysis with the selected metabolites indicated that methionine metabolism, which is related to H<jats:sub>2<\/jats:sub>S production, was the most frequently altered pathway. <jats:italic>H\u00a0pylori<\/jats:italic>\u2010inoculated cells produced more endogenous H<jats:sub>2<\/jats:sub>S than control cells. Moreover, ATCC 43504\u2010inoculated cells produced less H<jats:sub>2<\/jats:sub>S than ATCC 51932\u2010inoculated cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p><jats:italic>H\u00a0pylori<\/jats:italic> infection modulates endogenous H<jats:sub>2<\/jats:sub>S production in AGS cells, suggesting that H<jats:sub>2<\/jats:sub>S might be one of the bioactive molecules involved in the biological mechanisms of gastric mucosal disease including mucosal atrophy.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hel.12732","type":"journal-article","created":{"date-parts":[[2020,7,26]],"date-time":"2020-07-26T11:38:20Z","timestamp":1595763500000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["<i>Helicobacter pylori<\/i> infection modulates endogenous hydrogen sulfide production in gastric cancer AGS 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