幽门螺旋杆菌介导的自噬与胃癌发生机制的研究进展

Helicobacter pylori-mediated autophagy and gastric carcinogenesis

幽门螺旋杆菌(Helicobacter pylori,H.pylori)感染与慢性胃炎、消化性溃疡、胃肠化生和癌症的发生发展密切相关.其感染是多因素的,包括宿主的遗传易感性、基因调控、环境因素和H.pylori毒力因子的异质性.H.pylori通过多种黏附分子吸附于胃壁上,毒力因子逃避宿主的免疫反应,以及膜防御能力抵抗抗生素的杀伤,但目前H.pylori和人类宿主之间成功合作的各种机制尚未完全被阐明.自噬是一种细胞内通过形成双膜自噬体的自我降解过程,他在H.pylori感染的细胞内有重要作用.深入了解H.pylori毒力因子和宿主细胞之间的自噬过程及其分子机制,对于H.pylori诱导的自噬相关胃癌开启新途径有重要意义.

Helicobacter pylori（H. pylori） infection is closelyrelated to the development of chronic gastritis,peptic ulcer, gastrointestinal metaplasia, andgastric carcinogenesis. H. pylori infection is mul-tifactorial, including host genetic susceptibility,gene regulation, environmental factors and het-erogeneity of H. pylori virulence factors. H. pyloriadsorbs on the stomach wall through a varietyof adhesion molecules, evades the host immuneresponse through multiple virulence factors anddefends against the killing effects of antibioticskilling through the capability of membrane re-sistance. Currently, the cooperative mechanismsbetween H. pylori and the human host have notyet been fully elucidated. Recent studies haveshown that autophagy is an intracellular degradation process through the formation of double-membrane autophagosomes and plays an important role in H. pylori infection. Understanding of the process and molecular mechanisms of autophagy in host cells caused by H. pylori viru-lence factors will help better understand gastric carcinogenesis related to H. pylori-induced autophagy.