title: Inflammasome-mediated pyroptotic and apoptotic cell death, and defense against infection.
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.
authors.affiliation: Department of Microbiology and Immunology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
authors.forename: Youssef
authors.initials: Y
authors.lastname: Aachoui
authors.forename: Vitaliya
authors.initials: V
authors.lastname: Sagulenko
authors.forename: Edward A
authors.initials: EA
authors.lastname: Miao
authors.forename: Katryn J
authors.initials: KJ
authors.lastname: Stacey
mesh_terms: D000818:Animals; D020169:Caspases / Q000378:metabolism; D016923:Cell Death; D003141:Communicable Diseases / Q000276:immunology*; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D006801:Humans; D058847:Inflammasomes / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D015398:Signal Transduction
chemical_list: D016207:Cytokines; D058847:Inflammasomes; D020169:Caspases