Loop Between NLRP3 Inflammasome and Reactive Oxygen Species

Inflammasomes are cytosolic multiprotein complexes that mediate innate immune pathways. Inflammasomes activate inflammatory caspases and regulate inflammatory cytokines interleukin (IL)-1β and IL-18 as well as inflammatory cell death (pyroptosis). Among known inflammasomes, NLRP3 (NLR family pyrin d...

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Veröffentlicht in:Antioxidants & redox signaling Jg. 36; H. 10-12; S. 784
Hauptverfasser: Dominic, Abishai, Le, Nhat-Tu, Takahashi, Masafumi
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.04.2022
Schlagworte:
Inflammasomes - metabolism
Interleukin-1beta - metabolism
Macrophages - metabolism
NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
Pyroptosis
Reactive Oxygen Species - metabolism
pyroptosis
macrophages
cytokines
inflammation
mitochondria
interleukins
ISSN:1557-7716, 1557-7716
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Zusammenfassung:Inflammasomes are cytosolic multiprotein complexes that mediate innate immune pathways. Inflammasomes activate inflammatory caspases and regulate inflammatory cytokines interleukin (IL)-1β and IL-18 as well as inflammatory cell death (pyroptosis). Among known inflammasomes, NLRP3 (NLR family pyrin domain containing 3) inflammasome is unique and well studied owing to the fact that it senses a broad range of stimuli and is implicated in the pathogenesis of both microbial and sterile inflammatory diseases. Reactive oxygen species (ROS), especially derived from the mitochondria, are one of the critical mediators of NLRP3 inflammasome activation. Furthermore, NLRP3 inflammasome-driven inflammation recruits inflammatory cells, including macrophages and neutrophils, which in turn cause ROS production, suggesting a feedback loop between ROS and NLRP3 inflammasome. The precise mechanism of how ROS affects NLRP3 inflammasome activation still need to be addressed. This review will summarize the current knowledge on the molecular mechanisms underlying the activation of NLRP3 inflammasome with particular emphasis on the intricate balance of feedback loop between ROS and inflammasome activation. Understanding that this relationship is loop rather than traditionally understood linear mechanism will enable to fine-tune inflammasome activation under varied pathological settings. 36, 784-796.
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ISSN:1557-7716
1557-7716
DOI:10.1089/ars.2020.8257