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Helicobacter pylori infection modulates endogenous hydrogen sulfide production in gastric cancer AGS cells
Author(s) -
Kawahara Yoshinari,
Hirashita Yuka,
Tamura Chikako,
Kudo Yoko,
Sakai Kumiko,
Togo Kazumi,
Fukuda Kensuke,
Matsunari Osamu,
Okamoto Kazuhisa,
Ogawa Ryo,
Mizukami Kazuhiro,
Okimoto Tadayoshi,
Kodama Masaaki,
Murakami Kazunari
Publication year - 2020
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/hel.12732
Subject(s) - helicobacter pylori , caga , endogeny , microbiology and biotechnology , cell culture , chemistry , virulence , biology , biochemistry , gene , genetics
Background Persistent Helicobacter pylori infection induces gastric mucosal atrophy, which is a precancerous condition. Hydrogen sulfide (H 2 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 H pylori infection, we investigated the metabolic changes of gastric cancer cells co‐cultured with H pylori and observed the modulation of endogenous H 2 S production. Materials and Methods Gastric cancer AGS cells were co‐cultured with an H pylori 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‐tandem mass spectrometry (GC‐MS/MS). Orthogonal projections to latent structures discriminant analysis (OPLS‐DA) and pathway analysis were performed. In addition, intracellular H 2 S levels were measured by using HSip‐1 fluorescent probe. Results Results of OPLS‐DA showed a significant difference between the metabolism of untreated control cells and cells inoculated with the H pylori 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 2 S production, was the most frequently altered pathway. H pylori ‐inoculated cells produced more endogenous H 2 S than control cells. Moreover, ATCC 43504‐inoculated cells produced less H 2 S than ATCC 51932‐inoculated cells. Conclusions H pylori infection modulates endogenous H 2 S production in AGS cells, suggesting that H 2 S might be one of the bioactive molecules involved in the biological mechanisms of gastric mucosal disease including mucosal atrophy.

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