Fattinger Stefan A, Sellin Mikael E, Hardt Wolf-Dietrich
Institute of Microbiology, Department of Biology, ETH Zurich, Zurich, Switzerland; Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden.
Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden.
Curr Opin Microbiol. 2021 Feb;59:86-94. doi: 10.1016/j.mib.2020.09.014. Epub 2020 Oct 28.
The gut epithelium prevents bacterial access to the host's tissues and coordinates a number of mucosal defenses. Here, we review the function of epithelial inflammasomes in the infected host and focus on their role in defense against Salmonella Typhimurium. This pathogen employs flagella to swim towards the epithelium and a type III secretion system (TTSS) to dock and invade intestinal epithelial cells. Flagella and TTSS components are recognized by the canonical NAIP/NLRC4 inflammasome, while LPS activates the non-canonical Caspase-4/11 inflammasome. The relative contributions of these inflammasomes, the activated cell death pathways and the elicited mucosal defenses are subject to environmental control and appear to change along the infection trajectory. It will be an important future task to explain how this may enable defense against the challenges imposed by diverse bacterial enteropathogens.
肠道上皮组织可阻止细菌接触宿主组织,并协调多种黏膜防御机制。在此,我们综述上皮细胞炎性小体在受感染宿主中的功能,并着重探讨其在抵御鼠伤寒沙门氏菌中的作用。该病原体利用鞭毛向上皮组织游动,并通过III型分泌系统(TTSS)附着并侵入肠道上皮细胞。鞭毛和TTSS组件可被经典的NAIP/NLRC4炎性小体识别,而脂多糖则激活非经典的半胱天冬酶-4/11炎性小体。这些炎性小体的相对作用、激活的细胞死亡途径以及引发的黏膜防御均受环境控制,且似乎会随着感染进程而变化。解释这如何能够抵御多种细菌性肠道病原体带来的挑战将是未来一项重要的任务。