Institute for Molecular Bioscience, The University of Queensland, St Lucia 4072, Australia.
Curr Opin Microbiol. 2013 Jun;16(3):311-8. doi: 10.1016/j.mib.2013.02.004. Epub 2013 Mar 4.
Inflammasomes are multi-protein complexes that assemble in response to cellular infection, cellular stress or tissue damage. Inflammasomes provide signalling platforms for the activation of caspase-1, which in turn triggers lytic cell death and the maturation and secretion of the interleukins (IL), IL-1β and IL-18, which co-ordinate host-protective inflammatory responses. Recent studies also highlight emerging roles for interleukin-independent pathways in exerting microbial control. This article reviews cytokine-dependent and cytokine-independent host defence pathways engaged by inflammasomes during infection. Such inflammatory and antimicrobial mechanisms include the recruitment and activation of immune cells, the production of lipid mediators and complement proteins, the induction of the acute-phase and fever responses, the modulation of serum metallic ion content and the release of intracellular bacteria by pyroptotic cell death.
炎症小体是一种多蛋白复合物,可在细胞感染、细胞应激或组织损伤时组装。炎症小体为半胱氨酸蛋白酶-1 的激活提供信号平台,后者反过来又触发细胞裂解性死亡以及白细胞介素 (IL)、IL-1β 和 IL-18 的成熟和分泌,从而协调宿主保护性炎症反应。最近的研究还强调了白细胞介素非依赖性途径在发挥微生物控制方面的新作用。本文综述了炎症小体在感染过程中通过细胞因子依赖和细胞因子非依赖途径参与宿主防御。这些炎症和抗微生物机制包括免疫细胞的募集和激活、脂质介质和补体蛋白的产生、急性期和发热反应的诱导、血清金属离子含量的调节以及细胞焦亡性细胞死亡导致的细胞内细菌的释放。