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病原体对先天免疫炎症小体激活和细胞焦亡的调控作用

Subversion of inflammasome activation and pyroptosis by pathogenic bacteria.

机构信息

Department of Cell Biology, Ribeirão Preto Medical School, University of São Paulo (FMRP/USP) Ribeirão Preto, Brazil.

出版信息

Front Cell Infect Microbiol. 2013 Nov 26;3:76. doi: 10.3389/fcimb.2013.00076. eCollection 2013.

Abstract

Activation of the inflammasome occurs in response to a notably high number of pathogenic microbes and is a broad innate immune response that effectively contributes to restriction of pathogen replication and generation of adaptive immunity. Activation of these platforms leads to caspase-1- and/or caspase-11-dependent secretion of proteins, including cytokines, and induction of a specific form of cell death called pyroptosis, which directly or indirectly contribute for restriction of pathogen replication. Not surprisingly, bona fide intracellular pathogens developed strategies for manipulation of cell death to guarantee intracellular replication. In this sense, the remarkable advances in the knowledge of the inflammasome field have been accompanied by several reports characterizing the inhibition of this platform by several pathogenic bacteria. Herein, we review some processes used by pathogenic bacteria, including Yersinia spp., Pseudomonas aeruginosa, Vibrio parahaemolyticus, Chlamydia trachomatis, Francisella tularensis, Shigella flexneri, Legionella pneumophila, and Coxiella burnetii to evade the activation of the inflammasome and the induction of pyroptosis.

摘要

炎症小体的激活是对大量致病性微生物的反应,是一种广泛的先天免疫反应,可有效限制病原体的复制和产生适应性免疫。这些平台的激活导致半胱天冬酶-1 和/或半胱天冬酶-11 依赖性蛋白质(包括细胞因子)的分泌,并诱导一种称为细胞焦亡的特定形式的细胞死亡,其直接或间接地有助于限制病原体的复制。毫不奇怪,真正的细胞内病原体已经开发出操纵细胞死亡的策略,以保证细胞内复制。从这个意义上说,炎症小体领域的显著进展伴随着几项报道,这些报道描述了几种致病性细菌对该平台的抑制作用。在此,我们综述了一些致病性细菌(包括耶尔森菌属、铜绿假单胞菌、副溶血性弧菌、沙眼衣原体、土拉弗朗西斯菌、福氏志贺菌、嗜肺军团菌和贝氏柯克斯体)用来逃避炎症小体激活和细胞焦亡诱导的过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f95/3840304/a8a6fc4c7a76/fcimb-03-00076-g0001.jpg

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