Acetate Improves the Killing of Streptococcus ...
Type de document :
Compte-rendu et recension critique d'ouvrage
PMID :
Titre :
Acetate Improves the Killing of Streptococcus pneumoniae by Alveolar Macrophages via NLRP3 Inflammasome and Glycolysis-HIF-1α Axis
Auteur(s) :
Machado, Marina Gomes [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Universidade Federal de Minas Gerais = Federal University of Minas Gerais [Belo Horizonte, Brazil] [UFMG]
Patente, Thiago Andrade [Auteur]
Leiden University Medical Center [LUMC]
Rouillé, Yves [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Heumel, Severine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Melo, Eliza Mathias [Auteur]
Universidade Federal de Minas Gerais = Federal University of Minas Gerais [Belo Horizonte, Brazil] [UFMG]
Deruyter, Lucie [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Pourcet, Benoit [Auteur]
Récepteurs Nucléaires, Maladies Métaboliques et Cardiovasculaires - U 1011 [RNMCD]
Institut Européen de Génomique du Diabète - European Genomic Institute for Diabetes - FR 3508 [EGID]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Sencio, Valentin [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Teixeira, Mauro Martins [Auteur]
Universidade Federal de Minas Gerais = Federal University of Minas Gerais [Belo Horizonte, Brazil] [UFMG]
Trottein, François [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Universidade Federal de Minas Gerais = Federal University of Minas Gerais [Belo Horizonte, Brazil] [UFMG]
Patente, Thiago Andrade [Auteur]
Leiden University Medical Center [LUMC]
Rouillé, Yves [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Heumel, Severine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Melo, Eliza Mathias [Auteur]
Universidade Federal de Minas Gerais = Federal University of Minas Gerais [Belo Horizonte, Brazil] [UFMG]
Deruyter, Lucie [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Pourcet, Benoit [Auteur]
Récepteurs Nucléaires, Maladies Métaboliques et Cardiovasculaires - U 1011 [RNMCD]
Institut Européen de Génomique du Diabète - European Genomic Institute for Diabetes - FR 3508 [EGID]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Sencio, Valentin [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Teixeira, Mauro Martins [Auteur]
Universidade Federal de Minas Gerais = Federal University of Minas Gerais [Belo Horizonte, Brazil] [UFMG]
Trottein, François [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Titre de la revue :
Frontiers in Immunology
Pagination :
773261
Éditeur :
Frontiers
Date de publication :
2022-01-20
ISSN :
1664-3224
Mot(s)-clé(s) en anglais :
IL-1β
Streptococcus pneumoniae
alveolar macrophages
immunometabolism
innate immunity
nitric oxide
short chain fatty acid
Streptococcus pneumoniae
alveolar macrophages
immunometabolism
innate immunity
nitric oxide
short chain fatty acid
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Short-chain fatty acids (SCFAs) are metabolites produced mainly by the gut microbiota with a known role in immune regulation. Acetate, the major SCFA, is described to disseminate to distal organs such as lungs where it can ...
Lire la suite >Short-chain fatty acids (SCFAs) are metabolites produced mainly by the gut microbiota with a known role in immune regulation. Acetate, the major SCFA, is described to disseminate to distal organs such as lungs where it can arm sentinel cells, including alveolar macrophages, to fight against bacterial intruders. In the current study, we explored mechanisms through which acetate boosts macrophages to enhance their bactericidal activity. RNA sequencing analyses show that acetate triggers a transcriptomic program in macrophages evoking changes in metabolic process and immune effector outputs, including nitric oxide (NO) production. In addition, acetate enhances the killing activity of macrophages towards Streptococcus pneumoniae in an NO-dependent manner. Mechanistically, acetate improves IL-1β production by bacteria-conditioned macrophages and the latter acts in an autocrine manner to promote NO production. Strikingly, acetate-triggered IL-1β production was neither dependent of its cell surface receptor free-fatty acid receptor 2, nor of the enzymes responsible for its metabolism, namely acetyl-CoA synthetases 1 and 2. We found that IL-1β production by acetate relies on NLRP3 inflammasome and activation of HIF-1α, the latter being triggered by enhanced glycolysis. In conclusion, we unravel a new mechanism through which acetate reinforces the bactericidal activity of alveolar macrophages.Lire moins >
Lire la suite >Short-chain fatty acids (SCFAs) are metabolites produced mainly by the gut microbiota with a known role in immune regulation. Acetate, the major SCFA, is described to disseminate to distal organs such as lungs where it can arm sentinel cells, including alveolar macrophages, to fight against bacterial intruders. In the current study, we explored mechanisms through which acetate boosts macrophages to enhance their bactericidal activity. RNA sequencing analyses show that acetate triggers a transcriptomic program in macrophages evoking changes in metabolic process and immune effector outputs, including nitric oxide (NO) production. In addition, acetate enhances the killing activity of macrophages towards Streptococcus pneumoniae in an NO-dependent manner. Mechanistically, acetate improves IL-1β production by bacteria-conditioned macrophages and the latter acts in an autocrine manner to promote NO production. Strikingly, acetate-triggered IL-1β production was neither dependent of its cell surface receptor free-fatty acid receptor 2, nor of the enzymes responsible for its metabolism, namely acetyl-CoA synthetases 1 and 2. We found that IL-1β production by acetate relies on NLRP3 inflammasome and activation of HIF-1α, the latter being triggered by enhanced glycolysis. In conclusion, we unravel a new mechanism through which acetate reinforces the bactericidal activity of alveolar macrophages.Lire moins >
Langue :
Anglais
Vulgarisation :
Non
Source :
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