Department of Biology, Institute for Microbiology, Friedrich Alexander University Erlangen-Nuremberg, Erlangen, Germany.
Adv Exp Med Biol. 2019;1149:77-106. doi: 10.1007/5584_2019_360.
Helicobacter pylori represents a highly successful colonizer of the human stomach. Infections with this Gram-negative bacterium can persist lifelong, and although in the majority of cases colonization is asymptomatic, it can trigger pathologies ranging from chronic gastritis and peptic ulceration to gastric cancer. The interaction of the bacteria with the human host modulates immune responses in different ways to enable bacterial survival and persistence. H. pylori uses various pathogenicity-associated factors such as VacA, NapA, CGT, GGT, lipopolysaccharide, peptidoglycan, heptose 1,7-bisphosphate, ADP-heptose, cholesterol glucosides, urease and a type IV secretion system for controlling immune signaling and cellular functions. It appears that H. pylori manipulates multiple extracellular immune receptors such as integrin-β (CD18), EGFR, CD74, CD300E, DC-SIGN, MINCLE, TRPM2, T-cell and Toll-like receptors as well as a number of intracellular receptors including NLRP3, NOD1, NOD2, TIFA and ALPK1. Consequently, downstream signaling pathways are hijacked, inducing tolerogenic dendritic cells, inhibiting effector T cell responses and changing the gastrointestinal microbiota. Here, we discuss in detail the interplay of bacterial factors with multiple immuno-regulatory cells and summarize the main immune evasion and persistence strategies employed by H. pylori.
幽门螺杆菌是一种高度成功的人类胃部定植菌。这种革兰氏阴性细菌的感染可以终身持续，尽管在大多数情况下定植是无症状的，但它可以引发从慢性胃炎和消化性溃疡到胃癌等各种病理变化。细菌与人体宿主的相互作用以不同的方式调节免疫反应，以实现细菌的生存和持续。幽门螺杆菌使用各种与致病性相关的因子，如 VacA、NapA、CGT、GGT、脂多糖、肽聚糖、庚糖 1,7-双磷酸、ADP-庚糖、胆固醇糖苷、尿素酶和 IV 型分泌系统，来控制免疫信号和细胞功能。似乎幽门螺杆菌操纵多种细胞外免疫受体，如整合素-β（CD18）、EGFR、CD74、CD300E、DC-SIGN、MINCLE、TRPM2、T 细胞和 Toll 样受体，以及一些细胞内受体，包括 NLRP3、NOD1、NOD2、TIFA 和 ALPK1。因此，下游信号通路被劫持，诱导耐受树突状细胞，抑制效应 T 细胞反应，并改变胃肠道微生物群。在这里，我们详细讨论了细菌因子与多种免疫调节细胞的相互作用，并总结了幽门螺杆菌采用的主要免疫逃避和持续策略。
