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Interplay Between NLRP3 Inflammasome and Autophagy

The NLRP3 inflammasome is cytosolic multi-protein complex that induces inflammation and pyroptotic cell death in response to both pathogen (PAMPs) and endogenous activators (DAMPs). Recognition of PAMPs or DAMPs leads to formation of the inflammasome complex, which results in activation of caspase-1...

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Autores principales: Biasizzo, Monika, Kopitar-Jerala, Nataša
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7583715/
https://www.ncbi.nlm.nih.gov/pubmed/33163006
http://dx.doi.org/10.3389/fimmu.2020.591803
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author Biasizzo, Monika
Kopitar-Jerala, Nataša
author_facet Biasizzo, Monika
Kopitar-Jerala, Nataša
author_sort Biasizzo, Monika
collection PubMed
description The NLRP3 inflammasome is cytosolic multi-protein complex that induces inflammation and pyroptotic cell death in response to both pathogen (PAMPs) and endogenous activators (DAMPs). Recognition of PAMPs or DAMPs leads to formation of the inflammasome complex, which results in activation of caspase-1, followed by cleavage and release of pro-inflammatory cytokines. Excessive activation of NLRP3 inflammasome can contribute to development of inflammatory diseases and cancer. Autophagy is vital intracellular process for recycling and removal of damaged proteins and organelles, as well as destruction of intracellular pathogens. Cytosolic components are sequestered in a double-membrane vesicle—autophagosome, which then fuses with lysosome resulting in degradation of the cargo. The autophagy dysfunction can lead to diseases with hyperinflammation and excessive activation of NLRP3 inflammasome and thus acts as a major regulator of inflammasomes. Autophagic removal of NLRP3 inflammasome activators, such as intracellular DAMPs, NLRP3 inflammasome components, and cytokines can reduce inflammasome activation and inflammatory response. Likewise, inflammasome signaling pathways can regulate autophagic process necessary for balance between required host defense inflammatory response and prevention of excessive and detrimental inflammation. Autophagy has a protective role in some inflammatory diseases associated with NLRP3 inflammasome, including gouty arthritis, familial Mediterranean fever (FMF), and sepsis. Understanding the interregulation between these two essential biological processes is necessary to comprehend the biological mechanisms and designing possible treatments for multiple inflammatory diseases.
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spelling pubmed-75837152020-11-05 Interplay Between NLRP3 Inflammasome and Autophagy Biasizzo, Monika Kopitar-Jerala, Nataša Front Immunol Immunology The NLRP3 inflammasome is cytosolic multi-protein complex that induces inflammation and pyroptotic cell death in response to both pathogen (PAMPs) and endogenous activators (DAMPs). Recognition of PAMPs or DAMPs leads to formation of the inflammasome complex, which results in activation of caspase-1, followed by cleavage and release of pro-inflammatory cytokines. Excessive activation of NLRP3 inflammasome can contribute to development of inflammatory diseases and cancer. Autophagy is vital intracellular process for recycling and removal of damaged proteins and organelles, as well as destruction of intracellular pathogens. Cytosolic components are sequestered in a double-membrane vesicle—autophagosome, which then fuses with lysosome resulting in degradation of the cargo. The autophagy dysfunction can lead to diseases with hyperinflammation and excessive activation of NLRP3 inflammasome and thus acts as a major regulator of inflammasomes. Autophagic removal of NLRP3 inflammasome activators, such as intracellular DAMPs, NLRP3 inflammasome components, and cytokines can reduce inflammasome activation and inflammatory response. Likewise, inflammasome signaling pathways can regulate autophagic process necessary for balance between required host defense inflammatory response and prevention of excessive and detrimental inflammation. Autophagy has a protective role in some inflammatory diseases associated with NLRP3 inflammasome, including gouty arthritis, familial Mediterranean fever (FMF), and sepsis. Understanding the interregulation between these two essential biological processes is necessary to comprehend the biological mechanisms and designing possible treatments for multiple inflammatory diseases. Frontiers Media S.A. 2020-10-09 /pmc/articles/PMC7583715/ /pubmed/33163006 http://dx.doi.org/10.3389/fimmu.2020.591803 Text en Copyright © 2020 Biasizzo and Kopitar-Jerala. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Biasizzo, Monika
Kopitar-Jerala, Nataša
Interplay Between NLRP3 Inflammasome and Autophagy
title Interplay Between NLRP3 Inflammasome and Autophagy
title_full Interplay Between NLRP3 Inflammasome and Autophagy
title_fullStr Interplay Between NLRP3 Inflammasome and Autophagy
title_full_unstemmed Interplay Between NLRP3 Inflammasome and Autophagy
title_short Interplay Between NLRP3 Inflammasome and Autophagy
title_sort interplay between nlrp3 inflammasome and autophagy
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7583715/
https://www.ncbi.nlm.nih.gov/pubmed/33163006
http://dx.doi.org/10.3389/fimmu.2020.591803
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