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Cigarette smoke-induced gasdermin D activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on NLRP3

Chronic pulmonary inflammation and chronic obstructive pulmonary disease (COPD) are major health issues largely due to air pollution and cigarette smoke (CS) exposure. The role of the innate receptor NLRP3 (nucleotide-binding domain and leucine-rich repeat containing protein 3) orchestrating inflamm...

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Autores principales: Huot-Marchand, Sarah, Nascimento, Mégane, Culerier, Elodie, Bourenane, Mélissa, Savigny, Florence, Panek, Corinne, Serdjebi, Cindy, Le Bert, Marc, Quesniaux, Valérie F. J., Ryffel, Bernhard, Broz, Petr, Riteau, Nicolas, Gombault, Aurélie, Couillin, Isabelle
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9421433/
https://www.ncbi.nlm.nih.gov/pubmed/36045672
http://dx.doi.org/10.3389/fimmu.2022.918507
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author Huot-Marchand, Sarah
Nascimento, Mégane
Culerier, Elodie
Bourenane, Mélissa
Savigny, Florence
Panek, Corinne
Serdjebi, Cindy
Le Bert, Marc
Quesniaux, Valérie F. J.
Ryffel, Bernhard
Broz, Petr
Riteau, Nicolas
Gombault, Aurélie
Couillin, Isabelle
author_facet Huot-Marchand, Sarah
Nascimento, Mégane
Culerier, Elodie
Bourenane, Mélissa
Savigny, Florence
Panek, Corinne
Serdjebi, Cindy
Le Bert, Marc
Quesniaux, Valérie F. J.
Ryffel, Bernhard
Broz, Petr
Riteau, Nicolas
Gombault, Aurélie
Couillin, Isabelle
author_sort Huot-Marchand, Sarah
collection PubMed
description Chronic pulmonary inflammation and chronic obstructive pulmonary disease (COPD) are major health issues largely due to air pollution and cigarette smoke (CS) exposure. The role of the innate receptor NLRP3 (nucleotide-binding domain and leucine-rich repeat containing protein 3) orchestrating inflammation through formation of an inflammasome complex in CS-induced inflammation or COPD remains controversial. Using acute and subchronic CS exposure models, we found that Nlrp3-deficient mice or wild-type mice treated with the NLRP3 inhibitor MCC950 presented an important reduction of inflammatory cells recruited into the bronchoalveolar space and of pulmonary inflammation with decreased chemokines and cytokines production, in particular IL-1β demonstrating the key role of NLRP3. Furthermore, mice deficient for Caspase-1/Caspase-11 presented also decreased inflammation parameters, suggesting a role for the NLRP3 inflammasome. Importantly we showed that acute CS-exposure promotes NLRP3-dependent cleavage of gasdermin D in macrophages present in the bronchoalveolar space and in bronchial airway epithelial cells. Finally, Gsdmd-deficiency reduced acute CS-induced lung and bronchoalveolar space inflammation and IL-1β secretion. Thus, we demonstrated in our model that NLRP3 and gasdermin D are key players in CS-induced pulmonary inflammation and IL-1β release potentially through gasdermin D forming-pore and/or pyroptoctic cell death.
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spelling pubmed-94214332022-08-30 Cigarette smoke-induced gasdermin D activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on NLRP3 Huot-Marchand, Sarah Nascimento, Mégane Culerier, Elodie Bourenane, Mélissa Savigny, Florence Panek, Corinne Serdjebi, Cindy Le Bert, Marc Quesniaux, Valérie F. J. Ryffel, Bernhard Broz, Petr Riteau, Nicolas Gombault, Aurélie Couillin, Isabelle Front Immunol Immunology Chronic pulmonary inflammation and chronic obstructive pulmonary disease (COPD) are major health issues largely due to air pollution and cigarette smoke (CS) exposure. The role of the innate receptor NLRP3 (nucleotide-binding domain and leucine-rich repeat containing protein 3) orchestrating inflammation through formation of an inflammasome complex in CS-induced inflammation or COPD remains controversial. Using acute and subchronic CS exposure models, we found that Nlrp3-deficient mice or wild-type mice treated with the NLRP3 inhibitor MCC950 presented an important reduction of inflammatory cells recruited into the bronchoalveolar space and of pulmonary inflammation with decreased chemokines and cytokines production, in particular IL-1β demonstrating the key role of NLRP3. Furthermore, mice deficient for Caspase-1/Caspase-11 presented also decreased inflammation parameters, suggesting a role for the NLRP3 inflammasome. Importantly we showed that acute CS-exposure promotes NLRP3-dependent cleavage of gasdermin D in macrophages present in the bronchoalveolar space and in bronchial airway epithelial cells. Finally, Gsdmd-deficiency reduced acute CS-induced lung and bronchoalveolar space inflammation and IL-1β secretion. Thus, we demonstrated in our model that NLRP3 and gasdermin D are key players in CS-induced pulmonary inflammation and IL-1β release potentially through gasdermin D forming-pore and/or pyroptoctic cell death. Frontiers Media S.A. 2022-08-15 /pmc/articles/PMC9421433/ /pubmed/36045672 http://dx.doi.org/10.3389/fimmu.2022.918507 Text en Copyright © 2022 Huot-Marchand, Nascimento, Culerier, Bourenane, Savigny, Panek, Serdjebi, Le Bert, Quesniaux, Ryffel, Broz, Riteau, Gombault and Couillin https://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
Huot-Marchand, Sarah
Nascimento, Mégane
Culerier, Elodie
Bourenane, Mélissa
Savigny, Florence
Panek, Corinne
Serdjebi, Cindy
Le Bert, Marc
Quesniaux, Valérie F. J.
Ryffel, Bernhard
Broz, Petr
Riteau, Nicolas
Gombault, Aurélie
Couillin, Isabelle
Cigarette smoke-induced gasdermin D activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on NLRP3
title Cigarette smoke-induced gasdermin D activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on NLRP3
title_full Cigarette smoke-induced gasdermin D activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on NLRP3
title_fullStr Cigarette smoke-induced gasdermin D activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on NLRP3
title_full_unstemmed Cigarette smoke-induced gasdermin D activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on NLRP3
title_short Cigarette smoke-induced gasdermin D activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on NLRP3
title_sort cigarette smoke-induced gasdermin d activation in bronchoalveolar macrophages and bronchial epithelial cells dependently on nlrp3
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9421433/
https://www.ncbi.nlm.nih.gov/pubmed/36045672
http://dx.doi.org/10.3389/fimmu.2022.918507
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