Antimicrobial inflammasomes: unified signalling against diverse bacterial pathogens

被引:31
作者
Eldridge, Matthew J. G. [1 ]
Shenoy, Avinash R. [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Microbiol Sect, Med Res Council, Ctr Mol Bacteriol & Infect, London SW7 2AZ, England
关键词
NLRP3; INFLAMMASOME; IL-1-BETA PRODUCTION; MYCOBACTERIUM-TUBERCULOSIS; HOST-DEFENSE; CELL-DEATH; CASPASE-1; AUTOPROTEOLYSIS; SALMONELLA INFECTION; HUMAN MACROPHAGES; SECRETION SYSTEM; IMMUNE DEFENSE;
D O I
10.1016/j.mib.2014.10.008
中图分类号
Q93 [微生物学];
学科分类号
071005 [微生物学];
摘要
Inflammasomes - molecular platforms for caspase-1 activation - have emerged as common hubs for a number of pathways that detect and respond to bacterial pathogens. Caspase-1 activation results in the secretion of bioactive IL-1 beta and IL-18 and pyroptosis, and thus launches a systemic immune and inflammatory response. In this review we discuss signal transduction leading to 'canonical' and 'non-canonical' activation of caspase-1 through the involvement of upstream caspases. Recent studies have identified a growing number of regulatory networks involving guanylate binding proteins, protein kinases, ubiquitylation and necroptosis related pathways that modulate inflammasome responses and immunity to bacterial infection. By being able to respond to extracellular, vacuolar and cytosolic bacteria, their cytosolic toxins or ligands for cell surface receptors, inflammasomes have emerged as important sentinels of infection.
引用
收藏
页码:32 / 41
页数:10
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