The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation

The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage. However, the aberrant activation of the NLRP3 inflammasome has been linked...

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Published in	International journal of molecular sciences Vol. 20; no. 13; p. 3328
Main Authors	Kelley, Nathan, Jeltema, Devon, Duan, Yanhui, He, Yuan
Format	Journal Article
Language	English
Published	Switzerland MDPI AG 06.07.2019 MDPI
Subjects	Animals Apoptosis Cytokines Humans Immune system Inflammasomes - metabolism Kinases Ligands Mitochondria - pathology Mitochondrial DNA Models, Biological NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Pathogens Phosphorylation Protein Processing, Post-Translational Proteins Reactive Oxygen Species - metabolism Review Viral infections NLRP3 regulators Post-translational modification Mitochondrial dysfunction ROS Ionic flux Priming NLRP3 inflammasome Lysosomal damage
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Abstract	The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage. However, the aberrant activation of the NLRP3 inflammasome has been linked with several inflammatory disorders, which include cryopyrin-associated periodic syndromes, Alzheimer’s disease, diabetes, and atherosclerosis. The NLRP3 inflammasome is activated by diverse stimuli, and multiple molecular and cellular events, including ionic flux, mitochondrial dysfunction, and the production of reactive oxygen species, and lysosomal damage have been shown to trigger its activation. How NLRP3 responds to those signaling events and initiates the assembly of the NLRP3 inflammasome is not fully understood. In this review, we summarize our current understanding of the mechanisms of NLRP3 inflammasome activation by multiple signaling events, and its regulation by post-translational modifications and interacting partners of NLRP3.
AbstractList	The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage. However, the aberrant activation of the NLRP3 inflammasome has been linked with several inflammatory disorders, which include cryopyrin-associated periodic syndromes, Alzheimer’s disease, diabetes, and atherosclerosis. The NLRP3 inflammasome is activated by diverse stimuli, and multiple molecular and cellular events, including ionic flux, mitochondrial dysfunction, and the production of reactive oxygen species, and lysosomal damage have been shown to trigger its activation. How NLRP3 responds to those signaling events and initiates the assembly of the NLRP3 inflammasome is not fully understood. In this review, we summarize our current understanding of the mechanisms of NLRP3 inflammasome activation by multiple signaling events, and its regulation by post-translational modifications and interacting partners of NLRP3. The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage. However, the aberrant activation of the NLRP3 inflammasome has been linked with several inflammatory disorders, which include cryopyrin-associated periodic syndromes, Alzheimer's disease, diabetes, and atherosclerosis. The NLRP3 inflammasome is activated by diverse stimuli, and multiple molecular and cellular events, including ionic flux, mitochondrial dysfunction, and the production of reactive oxygen species, and lysosomal damage have been shown to trigger its activation. How NLRP3 responds to those signaling events and initiates the assembly of the NLRP3 inflammasome is not fully understood. In this review, we summarize our current understanding of the mechanisms of NLRP3 inflammasome activation by multiple signaling events, and its regulation by post-translational modifications and interacting partners of NLRP3.The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage. However, the aberrant activation of the NLRP3 inflammasome has been linked with several inflammatory disorders, which include cryopyrin-associated periodic syndromes, Alzheimer's disease, diabetes, and atherosclerosis. The NLRP3 inflammasome is activated by diverse stimuli, and multiple molecular and cellular events, including ionic flux, mitochondrial dysfunction, and the production of reactive oxygen species, and lysosomal damage have been shown to trigger its activation. How NLRP3 responds to those signaling events and initiates the assembly of the NLRP3 inflammasome is not fully understood. In this review, we summarize our current understanding of the mechanisms of NLRP3 inflammasome activation by multiple signaling events, and its regulation by post-translational modifications and interacting partners of NLRP3. [...]priming signals do not appear to affect the expression levels of ASC, pro-caspase-1, and pro-IL-18 [33]. [...]both signaling molecules MyD88 and TRIF of the NF-κB signaling pathway regulate the induction of NLRP3 and pro-IL-1β in response to TLR ligands [33]. [...]the priming signals regulate NLRP3 inflammasome activation through both transcription-dependent and -independent pathways (Figure 1). Furthermore, K+ efflux alone is capable of activating NLRP3, and high extracellular K+ blocks the activation of the NLRP3 inflammasome, but not the NLRC4 or AIM2 inflammasome [67,68]. [...]a decrease of intracellular K+ has been considered to be the common trigger for NLRP3 inflammasome activation [67]. [...]K+ efflux is also required for NLRP3 activation in the caspase-11-mediated non-canonical inflammasome pathway, but it is dispensable for the alternative NLRP3 inflammasome pathway [69,70,71].
Author	Jeltema, Devon Kelley, Nathan He, Yuan Duan, Yanhui
AuthorAffiliation	Department of Biochemistry, Microbiology and Immunology, Wayne State University School of Medicine, Detroit, MI 48201, USA
AuthorAffiliation_xml	– name: Department of Biochemistry, Microbiology and Immunology, Wayne State University School of Medicine, Detroit, MI 48201, USA
Author_xml	– sequence: 1 givenname: Nathan surname: Kelley fullname: Kelley, Nathan – sequence: 2 givenname: Devon surname: Jeltema fullname: Jeltema, Devon – sequence: 3 givenname: Yanhui surname: Duan fullname: Duan, Yanhui – sequence: 4 givenname: Yuan surname: He fullname: He, Yuan
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/31284572$$D View this record in MEDLINE/PubMed
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Snippet	The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines... [...]priming signals do not appear to affect the expression levels of ASC, pro-caspase-1, and pro-IL-18 [33]. [...]both signaling molecules MyD88 and TRIF of...
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SubjectTerms	Animals Apoptosis Cytokines Humans Immune system Inflammasomes - metabolism Kinases Ligands Mitochondria - pathology Mitochondrial DNA Models, Biological NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Pathogens Phosphorylation Protein Processing, Post-Translational Proteins Reactive Oxygen Species - metabolism Review Viral infections
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Title	The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation
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