Bacterial recognition pathways that lead to inflammasome activation

被引:101
作者
Storek, Kelly M. [1 ]
Monack, Denise M. [1 ]
机构
[1] Stanford Univ, Dept Microbiol & Immunol, Stanford, CA 94305 USA
基金
美国国家卫生研究院;
关键词
monocytes; macrophages; bacterial disease; inflammation; cytotoxicity; Toll-like receptors; pattern recognition receptors; signaling proteins; ENTERICA SEROVAR TYPHIMURIUM; CYTOSOLIC DNA SENSOR; INNATE IMMUNE RECOGNITION; CYCLIC GMP-AMP; I INTERFERON; NLRP3; INFLAMMASOME; HOST-DEFENSE; FRANCISELLA-TULARENSIS; MELANOMA; CASPASE-1; ACTIVATION;
D O I
10.1111/imr.12289
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammasomes are multi-protein signaling platforms that upon activation trigger the maturation of the pro-inflammatory cytokines, interleukin-1 (IL-1) and IL-18, and cell death. Inflammasome sensors detect microbial and host-derived molecules. Here, we review the mechanisms of inflammasome activation triggered by bacterial infection, primarily focusing on two model intracellular bacterial pathogens, Francisella novicida and Salmonella typhimurium. We discuss the complex relationship between bacterial recognition through direct and indirect detection by inflammasome sensors. We highlight regulation mechanisms that potentiate or limit inflammasome activation. We discuss the importance of caspase-1 and caspase-11 in host defense, and we examine the downstream consequences of inflammasome activation within the context of bacterial infections.
引用
收藏
页码:112 / 129
页数:18
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