| Summary: | 碩士 === 中國醫藥大學 === 基礎醫學研究所 === 97 === The ability of the Helicobacter pylori to survive in the interaction of non-phagocytes and phagocytes is postulated to enhance the persistence of this pathogen in the gastric mucosa and then to cause chronic inflammation. Nitric oxide (NO) production plays an important role in the gastric mucosal immune response to H. pylori and the associated inflammation. Pathogens might activate macrophage inducible nitric oxide synthase (iNOS) expression. The expression of iNOS is regulated in various cell types and can be enhanced by stimulation of bacterial lipopolysaccharide (LPS). In some pathogens, the ability to evade macrophage killing involves inducing rapid death of macrophages or suppression of macrophage activities. In this study, we used a mouse macrophage infection model to demonstrate that H. pylori could inhibit lipopolysaccharide (LPS)-induced NO production and iNOS expression. Analysis of iNOS specific mRNA and protein expression levels after infection revealed that H. pylori inhibited iNOS expression at both transcriptional and post-transcriptional levels, and only live and functional bacteria would do. Furthermore, this phenomenon involved down-regulation of mitogen-activated protein (MAP) kinase pathway, which triggered translocation of active nuclear factor (NF)-κB into nucleus. Our data suggested a new mechanism for H. pylori regulating innate immune responses of host cells to benefit persistent infection in host stomachs.
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