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Inflammasome-mediated pyroptotic and apoptotic cell death, and defense against infection
Open accessAbstract
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.
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“Casp11 deletion protects mice against a challenge with cytosol-invasive bacteria [612, 620]”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [612]
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“At a molecular level, pyroptosis generally relies on the activation of one or more caspases, including CASP1, CASP3, murine CASP11, and its human homologs CASP4 and CASP5, depending on the initiating stimulus [612, 613].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [612]
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Self-citation
Metadata
- Authors
- Aachoui, Y., Sagulenko, V., Miao, E. A., & Stacey, K. J.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- The University of Queensland (AU)
- Corresponding author
- Miao, Edward A
- Stacey, Katryn J
- Venue
- Current Opinion in Microbiology
- Publisher
- Elsevier BV
- Published
- 2013-06
- Volume
- 16
- Issue
- 3
- Pages
- 319-326
- ISSN
- 1369-5274 (ISSN-L)
- PMC
- PMC3742712
- OpenAlex
- W2077730689
- Cited by
- 296
- References
- 58
- Citations by year
- 2026: 13 · 2025: 16 · 2024: 22 · 2023: 30 · 2022: 39 · 2021: 32 · 2020: 24 · 2019: 29 · 2018: 19 · 2017: 17 · 2016: 14 · 2015: 21 · 2014: 13 · 2013: 7
- FWCI
- 1.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Microbiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Australian Research Council Future Fellowship (FT0991576)
- National Health and Medical Research Council (631472, 1010887)
- National Institute of Health (AI097518, AI057141)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- inflammasome, pyroptosis, apoptosis, caspase-1, caspase-11, NLRP3 inflammasome, NLRC4 inflammasome, AIM2 inflammasome, IL-1β, IL-18, procaspase-8, intracellular infection, host defense against infection
- MeSH terms
- Animals, Communicable Diseases, Humans, Signal Transduction, Cytokines, Cell Death, Caspases, Mice, Inflammasomes
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