炎性小体介导体细胞焦亡和细胞凋亡，以及抗感染防御。
Inflammasome-mediated pyroptotic and apoptotic cell death, and defense against infection.
机构信息
Department of Microbiology and Immunology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
出版信息
Curr Opin Microbiol. 2013 Jun;16(3):319-26. doi: 10.1016/j.mib.2013.04.004. Epub 2013 May 23.
Abstract
Cell death is an effective strategy to limit intracellular infections. Canonical inflammasomes, including NLRP3, NLRC4, and AIM2, recruit and activate caspase-1 in response to a range of microbial stimuli and endogenous danger signals. Caspase-1 then promotes the secretion of IL-1β and IL-18 and a rapid form of lytic programmed cell death termed pyroptosis. A second inflammatory caspase, mouse caspase-11, mediates pyroptotic death through an unknown non-canonical inflammasome system in response to cytosolic bacteria. In addition, recent work shows that inflammasomes can also recruit procaspase-8, initiating apoptosis. The induction of multiple pathways of cell death has probably evolved to counteract microbial evasion of cell death pathways.
摘要
细胞死亡是限制细胞内感染的一种有效策略。经典的炎症小体，包括 NLRP3、NLRC4 和 AIM2，可响应多种微生物刺激物和内源性危险信号招募并激活半胱天冬酶-1。半胱天冬酶-1 随后促进 IL-1β 和 IL-18 的分泌以及一种称为细胞焦亡的快速溶酶体程序性细胞死亡形式。第二种炎症半胱天冬酶，即鼠源半胱天冬酶-11，通过未知的非经典炎症小体系统对细胞质细菌作出反应，介导细胞焦亡。此外，最近的研究表明，炎症小体还可以招募起始凋亡的前半胱天冬酶-8。诱导多种细胞死亡途径的发生可能是为了对抗微生物逃避细胞死亡途径。
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本文引用的文献
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AIM2 and NLRP3 inflammasomes activate both apoptotic and pyroptotic death pathways via ASC.AIM2 和 NLRP3 炎性小体通过 ASC 激活细胞凋亡和细胞焦亡两条死亡通路。
Cell Death Differ. 2013 Sep;20(9):1149-60. doi: 10.1038/cdd.2013.37. Epub 2013 May 3.
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Caspase-11 protects against bacteria that escape the vacuole.Caspase-11 可以保护细胞免受逃离溶酶体的细菌的侵害。
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Caspase-11 stimulates rapid flagellin-independent pyroptosis in response to Legionella pneumophila.Caspase-11 可被 Legionella pneumophila 激活，从而引发依赖于 flagellin 的快速细胞焦亡。
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The Yersinia virulence effector YopM binds caspase-1 to arrest inflammasome assembly and processing.耶尔森氏菌毒力效应物 YopM 结合半胱天冬酶-1 以阻止炎症小体的组装和加工。
Cell Host Microbe. 2012 Dec 13;12(6):799-805. doi: 10.1016/j.chom.2012.10.020.
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NLRP1 inflammasome activation induces pyroptosis of hematopoietic progenitor cells.NLRP1 炎性小体激活诱导造血祖细胞发生细胞焦亡。
Immunity. 2012 Dec 14;37(6):1009-23. doi: 10.1016/j.immuni.2012.08.027. Epub 2012 Dec 6.
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Recognition of bacteria by inflammasomes.模式识别受体（PRRs）通过识别病原体相关分子模式（PAMPs）或损伤相关分子模式（DAMPs）来启动先天免疫反应。PAMPs 包括细菌、病毒和真菌细胞壁成分以及内毒素等，而 DAMPs 则是由细胞损伤或应激产生的分子。PRRs 家族包括 Toll 样受体（TLRs）、NOD 样受体（NLRs）和 RIG-I 样受体（RLRs）等。其中，NLRs 是最大的 PRR 家族之一，包含多个成员，如 NLRP1、NLRP3、NLRC4 和 AIM2 等。
NLRs 通过与 ASC（apoptosis-associated speck-like protein containing a caspase recruitment domain）形成炎性小体复合物来识别细菌。当 NLRs 识别到细菌时，它们会寡聚化并激活 caspase-1，后者进一步切割 pro-IL-1β 和 pro-IL-18，导致成熟的 IL-1β 和 IL-18 的释放。IL-1β 和 IL-18 是重要的促炎细胞因子，能够诱导炎症反应和免疫应答。
除了 NLRs，TLRs 也可以识别细菌。TLRs 是一类跨膜蛋白，能够识别细菌表面的 PAMPs，如 LPS（lipopolysaccharide）和肽聚糖等。TLRs 识别 PAMPs 后，会通过 MyD88（myeloid differentiation primary response 88）依赖性或独立途径激活 NF-κB（nuclear factor kappa-light-chain-enhancer of activated B cells）和 MAPK（mitogen-activated protein kinases）信号通路，导致炎症反应和免疫应答的发生。
总之，细菌通过被模式识别受体（PRRs）识别，引发先天免疫反应，包括细胞因子的释放和炎症反应的发生。
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CLEC5A is critical for dengue virus-induced inflammasome activation in human macrophages.CLEC5A 在登革热病毒诱导人巨噬细胞中的炎性体激活中起关键作用。
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TRIF licenses caspase-11-dependent NLRP3 inflammasome activation by gram-negative bacteria.TRIF 通过革兰氏阴性菌诱导 caspase-11 依赖的 NLRP3 炎性小体激活。
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