Pyroptosis: host cell death and inflammation

被引:3035
作者
Bergsbaken, Tessa [1 ]
Fink, Susan L. [2 ]
Cookson, Brad T. [1 ,3 ]
机构
[1] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA
[2] Univ Washington, Dept Mol & Cellular Biol, Seattle, WA 98195 USA
[3] Univ Washington, Dept Lab Med, Seattle, WA 98195 USA
基金
美国国家卫生研究院;
关键词
ANTHRAX LETHAL TOXIN; INTERLEUKIN-1-BETA CONVERTING-ENZYME; LEGIONELLA-PNEUMOPHILA INFECTION; MONOCYTE-DERIVED MACROPHAGES; MEDIATED IL-1-BETA SECRETION; ACUTE-RENAL-FAILURE; CASPASE-1; ACTIVATION; NALP3; INFLAMMASOME; DENDRITIC CELLS; CASPASE-1-DEPENDENT MECHANISM;
D O I
10.1038/nrmicro2070
中图分类号
Q93 [微生物学];
学科分类号
071005 [微生物学];
摘要
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.
引用
收藏
页码:99 / 109
页数:11
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