Lactate Inhibits the Pro-Inflammatory ...
Type de document :
Article dans une revue scientifique: Article original
PMID :
Titre :
Lactate Inhibits the Pro-Inflammatory Response and Metabolic Reprogramming in Murine Macrophages in a GPR81-Independent Manner.
Auteur(s) :
Errea, Agustina [Auteur]
Universidad Nacional de la Plata [Argentine] [UNLP]
Cayet, delphine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Marchetti, Philippe [Auteur]
Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 [JPArc]
Tang, Cong [Auteur]
Max Planck Institute for Heart and Lung Research [MPI-HLR]
Kluza, Jerome [Auteur]
Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 [JPArc]
Offermanns, Stefan [Auteur]
Max Planck Institute for Heart and Lung Research [MPI-HLR]
Sirard, Jean-Claude [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Rumbo, Martin [Auteur]
Universidad Nacional de la Plata [Argentine] [UNLP]
Universidad Nacional de la Plata [Argentine] [UNLP]
Cayet, delphine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Marchetti, Philippe [Auteur]

Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 [JPArc]
Tang, Cong [Auteur]
Max Planck Institute for Heart and Lung Research [MPI-HLR]
Kluza, Jerome [Auteur]

Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer - U837 [JPArc]
Offermanns, Stefan [Auteur]
Max Planck Institute for Heart and Lung Research [MPI-HLR]
Sirard, Jean-Claude [Auteur]

Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Rumbo, Martin [Auteur]
Universidad Nacional de la Plata [Argentine] [UNLP]
Titre de la revue :
PLOS ONE
Pagination :
e0163694
Éditeur :
Public Library of Science
Date de publication :
2016-11-15
ISSN :
1932-6203
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Lactate is an essential component of carbon metabolism in mammals. Recently, lactate was shown to signal through the G protein coupled receptor 81 (GPR81) and to thus modulate inflammatory processes. This study demonstrates ...
Lire la suite >Lactate is an essential component of carbon metabolism in mammals. Recently, lactate was shown to signal through the G protein coupled receptor 81 (GPR81) and to thus modulate inflammatory processes. This study demonstrates that lactate inhibits pro-inflammatory signaling in a GPR81-independent fashion. While lipopolysaccharide (LPS) triggered expression of IL-6 and IL-12 p40, and CD40 in bone marrow-derived macrophages, lactate was able to abrogate these responses in a dose dependent manner in Gpr81-/- cells as well as in wild type cells. Macrophage activation was impaired when glycolysis was blocked by chemical inhibitors. Remarkably, lactate was found to inhibit LPS-induced glycolysis in wild type as well as in Gpr81-/- cells. In conclusion, our study suggests that lactate can induce GPR81-independent metabolic changes that modulate macrophage pro-inflammatory activation.Lire moins >
Lire la suite >Lactate is an essential component of carbon metabolism in mammals. Recently, lactate was shown to signal through the G protein coupled receptor 81 (GPR81) and to thus modulate inflammatory processes. This study demonstrates that lactate inhibits pro-inflammatory signaling in a GPR81-independent fashion. While lipopolysaccharide (LPS) triggered expression of IL-6 and IL-12 p40, and CD40 in bone marrow-derived macrophages, lactate was able to abrogate these responses in a dose dependent manner in Gpr81-/- cells as well as in wild type cells. Macrophage activation was impaired when glycolysis was blocked by chemical inhibitors. Remarkably, lactate was found to inhibit LPS-induced glycolysis in wild type as well as in Gpr81-/- cells. In conclusion, our study suggests that lactate can induce GPR81-independent metabolic changes that modulate macrophage pro-inflammatory activation.Lire moins >
Langue :
Anglais
Comité de lecture :
Oui
Audience :
Internationale
Vulgarisation :
Non
Source :
Fichiers
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5112849/pdf
- Accès libre
- Accéder au document
- Accès libre
- Accéder au document