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细菌感染过程中炎症小体和细胞焦亡的激活与调控。

Activation and manipulation of inflammasomes and pyroptosis during bacterial infections.

机构信息

Department of Biochemistry, University of Lausanne, Epalinges, Switzerland.

出版信息

Biochem J. 2022 Apr 14;479(7):867-882. doi: 10.1042/BCJ20220051.

Abstract

Following detection of pathogen infection and disrupted cellular homeostasis, cells can activate a range of cell death pathways, such as apoptosis, necroptosis and pyroptosis, as part of their defence strategy. The initiation of pro-inflammatory, lytic pyroptosis is controlled by inflammasomes, which respond to a range of cellular perturbations. As is true for many host defence pathways, pathogens have evolved multiple mechanisms to subvert this pathway, many of which have only recently been described. Herein, we will discuss the mechanisms by which inflammasomes sense pathogen invasion and initiate pyroptosis and the effector mechanisms used by pathogens to suppress this pathway and preserve their niche.

摘要

在检测到病原体感染和细胞内稳态破坏后,细胞可以激活一系列细胞死亡途径,如细胞凋亡、坏死性凋亡和细胞焦亡,作为其防御策略的一部分。促炎、裂解性细胞焦亡的启动受炎性小体控制,炎性小体可响应多种细胞扰动。与许多宿主防御途径一样,病原体已经进化出多种机制来颠覆这种途径,其中许多机制直到最近才被描述。在此,我们将讨论炎性小体感知病原体入侵并启动细胞焦亡的机制,以及病原体用来抑制该途径并维持其生态位的效应机制。

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