Quantifying Cell Death Induced by the NLRC4 Inflammasome.
Cell death
Flatox
Inflammasome
Macrophages
NAIP
NLRC4
Needletox
Pyroptosis
Journal
Methods in molecular biology (Clifton, N.J.)
ISSN: 1940-6029
Titre abrégé: Methods Mol Biol
Pays: United States
ID NLM: 9214969
Informations de publication
Date de publication:
2023
2023
Historique:
medline:
15
8
2023
pubmed:
14
8
2023
entrez:
14
8
2023
Statut:
ppublish
Résumé
The Nod-like Receptor (NLR) apoptosis inhibitory proteins (NAIPs) are cytosolic receptors that sense cytosolic bacterial proteins. NAIP ligation induces its association with NLRC4, leading to the assembly of the NAIP/NLRC4 inflammasome, which induces the activation of the caspase-1 protease. Caspase-1 then cleaves pro-interleukin (IL)-1β, pro-IL-18, and gasdermin D and induces a form of pro-inflammatory cell death, pyroptosis. These processes culminate in host defense against bacterial infection. Here we describe methods for activating NAIP/NLRC4 inflammasome signalling in human and murine macrophages and quantifying inflammasome-induced cell death.
Identifiants
pubmed: 37578724
doi: 10.1007/978-1-0716-3350-2_13
doi:
Substances chimiques
Inflammasomes
0
Calcium-Binding Proteins
0
Apoptosis Regulatory Proteins
0
Caspases
EC 3.4.22.-
Caspase 1
EC 3.4.22.36
NLRC4 protein, human
0
CARD Signaling Adaptor Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
199-210Informations de copyright
© 2023. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.
Références
Martinon F, Burns K, Tschopp J (2002) The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta. Mol Cell 10:417–426
doi: 10.1016/S1097-2765(02)00599-3
pubmed: 12191486
Boucher D, Monteleone M, Coll RC et al (2018) Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity. J Exp Med 215:827–840. https://doi.org/10.1084/jem.20172222
doi: 10.1084/jem.20172222
pubmed: 29432122
pmcid: 5839769
Chan AH, Schroder K (2020) Inflammasome signaling and regulation of interleukin-1 family cytokines. J Exp Med 217:e20190314. https://doi.org/10.1084/jem.20190314
doi: 10.1084/jem.20190314
pubmed: 31611248
Rauch I, Tenthorey JL, Nichols RD et al (2016) NAIP proteins are required for cytosolic detection of specific bacterial ligands in vivo. J Exp Med 213:657–665. https://doi.org/10.1084/jem.20151809
doi: 10.1084/jem.20151809
pubmed: 27045008
pmcid: 4854734
Zhao Y, Yang J, Shi J et al (2011) The NLRC4 inflammasome receptors for bacterial flagellin and type III secretion apparatus. Nature 477:596–600. https://doi.org/10.1038/nature10510
doi: 10.1038/nature10510
pubmed: 21918512
Kofoed EM, Vance RE (2011) Innate immune recognition of bacterial ligands by NAIPs determines inflammasome specificity. Nature 477:592–595. https://doi.org/10.1038/nature10394
doi: 10.1038/nature10394
pubmed: 21874021
pmcid: 3184209
Yang J, Zhao Y, Shi J, Shao F (2013) Human NAIP and mouse NAIP1 recognize bacterial type III secretion needle protein for inflammasome activation. Proc Natl Acad Sci 110:14408–14413. https://doi.org/10.1073/pnas.1306376110
doi: 10.1073/pnas.1306376110
pubmed: 23940371
pmcid: 3761597
von Moltke J, Trinidad NJ, Moayeri M et al (2012) Rapid induction of inflammatory lipid mediators by the inflammasome in vivo. Nature 490:107–111. https://doi.org/10.1038/nature11351
doi: 10.1038/nature11351
Kuida K, Lippke JA, Ku G et al (1995) Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme. Science 267:2000–2003. https://doi.org/10.1126/science.7535475
doi: 10.1126/science.7535475
pubmed: 7535475
Chen KW, Monteleone M, Boucher D et al (2018) Noncanonical inflammasome signaling elicits gasdermin D-dependent neutrophil extracellular traps. Sci Immunol 3. https://doi.org/10.1126/sciimmunol.aar6676
Linton SD (2005) Caspase inhibitors: a pharmaceutical industry perspective. Curr Top Med Chem 5:1697–1717. https://doi.org/10.2174/156802605775009720
doi: 10.2174/156802605775009720
pubmed: 16375749