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首页> 外文期刊>Current opinion in gastroenterology >Helicobacter pylori infection: pathogenesis
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Helicobacter pylori infection: pathogenesis

机译：幽门螺杆菌感染：发病机理

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This review covers progress in identifying Helicobacter pylori-derived factors that are involved in survival and virulence of the organism and in elucidating host response pathways that can limit the infection but are also susceptible to dysregulation. Recent work has identified genes of the cytotoxin-associated gene (cag) pathogenicity island (PAI) involved in regulating signaling, interleukin-8 secretion, and phenotypic events in epithelial cells. New roles in pathogenesis have been recognized for vacuolating toxin A (VacA) and urease, H. pylori membrane and secreted factors, and host epithelial surface molecules. Molecular pathways involved in H. pylori-induced apoptosis in epithelial cells, T cells, and macrophages are being dissected. Activation of toll-like receptors and bacterial factors involved in nitric oxide (NO) and reactive oxygen species induction were also described. The ability of H. pylori to limit NO production by several mechanisms may be an important part of its ability to evade the host immune response. Cum Opin Gastroenteroi 2003,
机译：这篇综述涵盖了在鉴定幽门螺杆菌来源的因素方面的进展，这些因素与该生物的存活和毒力有关，并且阐明了可以限制感染但也容易失调的宿主反应途径。最近的工作已经确定了细胞毒素相关基因（cag）致病岛（PAI）的基因，这些基因参与调节上皮细胞的信号传导，白介素8分泌和表型事件。已经认识到在空化毒素A（VacA）和脲酶，幽门螺杆菌膜和分泌因子以及宿主上皮表面分子方面具有新的作用。正在剖析参与幽门螺杆菌诱导的上皮细胞，T细胞和巨噬细胞凋亡的分子途径。还介绍了涉及一氧化氮（NO）和活性氧物种诱导的收费型受体和细菌因子的激活。幽门螺杆菌通过几种机制限制NO产生的能力可能是其规避宿主免疫反应能力的重要组成部分。暨美食胃肠2003，

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