Bergsbaken Tessa, Fink Susan L, Cookson Brad T
Department of Microbiology, University of Washington, Seattle, Washington 98195, USA.
Nat Rev Microbiol. 2009 Feb;7(2):99-109. doi: 10.1038/nrmicro2070.
Eukaryotic cells can initiate several distinct programmes of self-destruction, and the nature of the cell death process (non-inflammatory or proinflammatory) instructs responses of neighbouring cells, which in turn dictates important systemic physiological outcomes. Pyroptosis, or caspase 1-dependent cell death, is inherently inflammatory, is triggered by various pathological stimuli, such as stroke, heart attack or cancer, and is crucial for controlling microbial infections. Pathogens have evolved mechanisms to inhibit pyroptosis, enhancing their ability to persist and cause disease. Ultimately, there is a competition between host and pathogen to regulate pyroptosis, and the outcome dictates life or death of the host.
真核细胞可以启动几种不同的自我毁灭程序,细胞死亡过程的性质(非炎症性或促炎症性)指导邻近细胞的反应,而这反过来又决定了重要的全身生理结果。细胞焦亡,即半胱天冬酶1依赖性细胞死亡,本质上具有炎症性,由各种病理刺激引发,如中风、心脏病发作或癌症,对于控制微生物感染至关重要。病原体已经进化出抑制细胞焦亡的机制,从而增强它们持续存在和致病的能力。最终,宿主和病原体之间存在调节细胞焦亡的竞争,其结果决定了宿主的生死。