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Gene expression changes in gastric epithelial cells induced by Helicobacter pylori infection

ABSTRACT: This group is focusing on the molecular mechanisms of the biosynthesis of glycoconjugates and carbohydrate ligands important in the process of gastric carcinogenesis and on gastric carcinoma progression and metastasis. The adhesion of H. pylori to epithelial cells induces a variety of modifications, including changes in cell morphology,cytokine production and release, alterations in glycosylation and in the biosynthesis of mucins. This study aims to identify the gene expression changes in the gastric epithelial cells (AGS) induced by Helicobacter pylori infection. This experiment was performed as previously described in the literature by submitting a gastric cell line to co-culture with reference strains of H. pylori.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE27347 | GEO | 2011/02/17

SECONDARY ACCESSION(S): PRJNA137413

REPOSITORIES: GEO

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Project description:Background: Helicobacter pylori is an important human pathogen that infects the human gastric mucosa leading to chronic inflammation which is responsible for severe gastroduodenal diseases. The Outer Inflammatory Protein A (OipA) of H. pylori is an important virulence factor. However, the role of OipA in gastric cancer and ulcer development is still not well-established. Phase variation within a CT dinucleotide repeat motif of oipA switches its expression “on” and “off”. This study aims to elucidate the role of OipA in H. pylori infection using oipA “on” and “off” clinical strains and oipA deletion mutant. Methods: Proteomics analysis was performed on AGS human gastric epithelial cell line post-infection with oipA “on” and “off” H. pylori using liquid chromatography / mass spectrometry (LC/MS). In addition, AGS apoptosis and cell cycle assays were performed. To confirm the findings, oipA deletion mutant (ΔoipA) was generated and expression of VacA was detected using Western blotting. Result: Expression of AGS proteins involve in human disease was suppressed / down-regulated post-infection with oipA “off” strains, as well as oipA mutant, compared to oipA “on” strains. Furthermore, oipA “off” strains and oipA mutant resulted in a higher level of apoptosis and G0/G1 cell-cycle arrest in AGS cells than oipA “on” strains. Interestingly, deletion of oipA was found to increase VacA production by the bacterium. Discussion: The capability of oipA “off” strains to induce apoptosis and suppress proteins having roles in human disease may suggest that these H. pylori may be less virulent or may even be protective against carcinogenesis compared to its oipA “on” counterparts. This may potentially explain the higher incidence of gastric cancer among East Asian which oipA “on” strains predominates. Conclusions: Data from this study strengthened our understanding of the role of H. pylori OipA as a virulence factor in chronic inflammation, metastasis and carcinogenesis.

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Gene expression changes in gastric epithelial cells induced by Helicobacter pylori infection

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