Storek Kelly M, Monack Denise M
Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA.
Immunol Rev. 2015 May;265(1):112-29. doi: 10.1111/imr.12289.
Inflammasomes are multi-protein signaling platforms that upon activation trigger the maturation of the pro-inflammatory cytokines, interleukin-1β (IL-1β) 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.
炎性小体是多蛋白信号平台，激活后可触发促炎细胞因子白细胞介素-1β（IL-1β）和IL-18的成熟以及细胞死亡。炎性小体传感器可检测微生物和宿主来源的分子。在此，我们综述由细菌感染触发的炎性小体激活机制，主要聚焦于两种典型的细胞内细菌病原体，即新凶手弗朗西斯菌和鼠伤寒沙门氏菌。我们讨论了炎性小体传感器通过直接和间接检测进行细菌识别之间的复杂关系。我们强调增强或限制炎性小体激活的调节机制。我们讨论了半胱天冬酶-1和半胱天冬酶-11在宿主防御中的重要性，并在细菌感染的背景下研究炎性小体激活的下游后果。
