Department of Molecular Bacteriology and Immunology, Graduate School of Medicine, University of the Ryukyus, Nishihara, Okinawa 903-0125, Japan.
Trends Microbiol. 2013 Jul;21(7):342-9. doi: 10.1016/j.tim.2013.04.005. Epub 2013 May 24.
The inflammasome is composed of nucleotide-binding, oligomerization domain (NOD)-like receptor (NLR) proteins, and leads to caspase-1 activation and subsequent secretion of the proinflammatory cytokines interleukin 1β (IL-1β) and interleukin-18 (IL-18). After certain pathogenic bacteria infect host cells, such as macrophages, NLR-mediated inflammasome activation is triggered to form part of the host defenses against the invading pathogens. However, recent evidence has shown that bacteria have strategies for evading inflammasome activation in host cells. In this review, we focus on NLR-mediated inflammasome activation and bacterial evasion of the inflammasome as part of the battle between the host defenses and pathogens.
炎症小体由核苷酸结合寡聚化结构域（NOD）样受体（NLR）蛋白组成，导致半胱天冬酶-1 的激活，随后促炎细胞因子白细胞介素 1β（IL-1β）和白细胞介素 18（IL-18）的分泌。在某些致病性细菌感染宿主细胞（如巨噬细胞）后，NLR 介导的炎症小体激活被触发，形成宿主防御机制的一部分，以对抗入侵的病原体。然而，最近的证据表明，细菌有策略来逃避宿主细胞中的炎症小体激活。在这篇综述中，我们重点关注 NLR 介导的炎症小体激活和细菌逃避炎症小体作为宿主防御和病原体之间斗争的一部分。
