Inflammasome-mediated pyroptotic and apoptotic cell death, and defense against infection.

Journal Article (Review;Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Aachoui, Y; Sagulenko, V; Miao, EA; Stacey, KJ

Published Date

  • June 2013

Published In

Volume / Issue

  • 16 / 3

Start / End Page

  • 319 - 326

PubMed ID

  • 23707339

Pubmed Central ID

  • PMC3742712

Electronic International Standard Serial Number (EISSN)

  • 1879-0364

International Standard Serial Number (ISSN)

  • 1369-5274

Digital Object Identifier (DOI)

  • 10.1016/j.mib.2013.04.004

Language

  • eng