Interaction of Mycobacteria With Host Cell Inflammasomes.
Interaction of Mycobacteria With Host Cell Inflammasomes.
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DOI：
10.3389/fimmu.2022.791136
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发表时间：
2022
影响因子：
7.3
通讯作者：
Briken V
中科院分区：
文献类型：
--
作者：
Rastogi S;Briken V
炎性小体复合物对于宿主防御细胞内细菌感染是重要的。结核分枝杆菌（Mycobacterium tuberculosis，Mtb）是一种兼性胞内细菌，能够在感染的巨噬细胞中存活。在这里，我们讨论了宿主细胞炎性小体如何感测结核分枝杆菌和其他相关的分枝杆菌物种。此外，我们描述了NLRP 3炎性小体传感Mtb的分子机制，其涉及VII型分泌系统ESX-1、细胞表面脂质（TDM/TDB）、分泌的效应蛋白（LpqH、PPE 13、EST 12、EsxA）和作用于炎性小体激活的引发和/或激活步骤的双链RNA。相比之下，Mtb还通过经由其水解酶Hip 1限制细胞表面配体的暴露、通过经由分泌的Mtb效应子Rv 3364 c抑制宿主细胞组织蛋白酶G蛋白酶以及最后通过经由其丝氨酸/苏氨酸激酶PknF限制细胞内触发物（K+和Cl-流出以及细胞溶质活性氧种类产生）来介导NLRP 3炎性体的抑制。此外，Mtb通过未知的机制抑制AIM 2炎性小体活化。总的来说，有很好的证据表明，Mtb试图限制炎性小体激活，而宿主细胞试图感知Mtb并激活炎性小体，这两者之间存在拔河。详细的分子机制和炎性小体激活对结核分枝杆菌毒力或宿主易感性的重要性尚未得到充分研究。
The inflammasome complex is important for host defense against intracellular bacterial infections. Mycobacterium tuberculosis (Mtb) is a facultative intracellular bacterium which is able to survive in infected macrophages. Here we discuss how the host cell inflammasomes sense Mtb and other related mycobacterial species. Furthermore, we describe the molecular mechanisms of NLRP3 inflammasome sensing of Mtb which involve the type VII secretion system ESX-1, cell surface lipids (TDM/TDB), secreted effector proteins (LpqH, PPE13, EST12, EsxA) and double-stranded RNA acting on the priming and/or activation steps of inflammasome activation. In contrast, Mtb also mediates inhibition of the NLRP3 inflammasome by limiting exposure of cell surface ligands via its hydrolase, Hip1, by inhibiting the host cell cathepsin G protease via the secreted Mtb effector Rv3364c and finally, by limiting intracellular triggers (K+ and Cl- efflux and cytosolic reactive oxygen species production) via its serine/threonine kinase PknF. In addition, Mtb inhibits the AIM2 inflammasome activation via an unknown mechanism. Overall, there is good evidence for a tug-of-war between Mtb trying to limit inflammasome activation and the host cell trying to sense Mtb and activate the inflammasome. The detailed molecular mechanisms and the importance of inflammasome activation for virulence of Mtb or host susceptibility have not been fully investigated.
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