Division of Human Biology, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Mailstop C3-168, Seattle, Washington 981091024, USA.
Nat Rev Microbiol. 2013 Jun;11(6):385-99. doi: 10.1038/nrmicro3016. Epub 2013 May 8.
The bacterial pathogen Helicobacter pylori has co-evolved with humans and colonizes approximately 50% of the human population, but only causes overt gastric disease in a subset of infected hosts. In this Review, we discuss the pathogenesis of H. pylori and the mechanisms it uses to promote persistent colonization of the gastric mucosa, with a focus on recent insights into the role of the virulence factors vacuolating cytotoxin (VacA), cytotoxin-associated gene A (CagA) and CagL. We also describe the immunobiology of H. pylori infection and highlight how this bacterium manipulates the innate and adaptive immune systems of the host to promote its own persistence.
细菌病原体幽门螺杆菌与人类共同进化,定植于约 50%的人类人口中,但仅在一部分受感染宿主中引起明显的胃部疾病。在这篇综述中,我们讨论了幽门螺杆菌的发病机制及其用于促进胃黏膜持续定植的机制,重点是最近对毒力因子空泡细胞毒素(VacA)、细胞毒素相关基因 A(CagA)和 CagL 作用的认识。我们还描述了幽门螺杆菌感染的免疫生物学,并强调了这种细菌如何操纵宿主的先天和适应性免疫系统以促进自身的持续存在。