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Upregulation of inducible nitric oxide synthase and nitric oxide in Helicobacter pylori-infected human gastric epithelial cells Possible role of interferon-gamma in polarized nitric oxide secretion



Upregulation of inducible nitric oxide synthase and nitric oxide in Helicobacter pylori-infected human gastric epithelial cells Possible role of interferon-gamma in polarized nitric oxide secretion



Abstracts of the General Meeting of the American Society for Microbiology 101: 311-312



Background: Gastric epithelial cells can provide signals that initiate an acute mucosal inflammatory response following H. pylori infection. Nitric oxide (NO) generated by nitric oxide synthase (NOS) is known to be an important modulator of the mucosal inflammatory response. In this study, we questioned whether H. pylori infection could upregulate the epithelial cell inducible NOS (iNOS) gene expression and whether NO production could show polarity that can be regulated by immune mediators. Methods: Human gastric epithelial cell lines were infected with H. pylori, and the iNOS mRNA expression was assessed by quantitative RT-PCR. NO production was assayed by determining nitrite/nitrate levels in culture supernatants. To study the MAP kinase involvement for NO up-regulation, H. pylori-infected cells were treated with specific MAP kinase inhibitors. To determine the polarity of NO secretion by the H. pylori-infected epithelial cells, Caco-2 cells were cultured as polarized monolayers in transwell chambers, and NO production was measured. Results: iNOS mRNA levels were significantly upregulated in the cells infected with H. pylori, and expression of iNOS protein was confirmed by Western blot analysis. Increased NO production in the gastric epithelial cells was seen as early as 12 h post-infection, and reached maximal levels by 24 h post-infection. The specific MAP kinase inhibitors decreased H. pylori-induced iNOS and NO up-regulation. After H. pylori infection of polarized epithelial cells, NO was released predominantly into the apical compartment, and IL-8 was released predominantly into the basolateral compartment. The addition of IFN-gamma to H. pylori-infected polarized epithelial cells showed a synergistically higher apical and basolateral NO release. Conclusion: These results suggest that NO production in H. pylori-infected gastric epithelial cells may play a role in the modulation of gastric mucosal inflammation.

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