Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner

Autores
Errea, Agustina Juliana; Cayet, Delphine; Marchetti, Philippe; Tang, Cong; Kluza, Jerome; Offermanns, Stefan; Sirard, Jean-Claude; Rumbo, Martín
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
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.
Instituto de Estudios Inmunológicos y Fisiopatológicos
Materia
Ciencias Médicas
Lactate
GPR81
Macrophage pro-inflammatory
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/85969
Acceder
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oai_identifier_str oai:sedici.unlp.edu.ar:10915/85969
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent mannerErrea, Agustina JulianaCayet, DelphineMarchetti, PhilippeTang, CongKluza, JeromeOffermanns, StefanSirard, Jean-ClaudeRumbo, MartínCiencias MédicasLactateGPR81Macrophage pro-inflammatoryLactate 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.Instituto de Estudios Inmunológicos y Fisiopatológicos2016info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/85969enginfo:eu-repo/semantics/altIdentifier/issn/1932-6203info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0164098info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-10-22T16:57:33Zoai:sedici.unlp.edu.ar:10915/85969Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-10-22 16:57:33.359SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner
title Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner
spellingShingle Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner
Errea, Agustina Juliana
Ciencias Médicas
Lactate
GPR81
Macrophage pro-inflammatory
title_short Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner
title_full Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner
title_fullStr Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner
title_full_unstemmed Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner
title_sort Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner
dc.creator.none.fl_str_mv Errea, Agustina Juliana
Cayet, Delphine
Marchetti, Philippe
Tang, Cong
Kluza, Jerome
Offermanns, Stefan
Sirard, Jean-Claude
Rumbo, Martín
author Errea, Agustina Juliana
author_facet Errea, Agustina Juliana
Cayet, Delphine
Marchetti, Philippe
Tang, Cong
Kluza, Jerome
Offermanns, Stefan
Sirard, Jean-Claude
Rumbo, Martín
author_role author
author2 Cayet, Delphine
Marchetti, Philippe
Tang, Cong
Kluza, Jerome
Offermanns, Stefan
Sirard, Jean-Claude
Rumbo, Martín
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Ciencias Médicas
Lactate
GPR81
Macrophage pro-inflammatory
topic Ciencias Médicas
Lactate
GPR81
Macrophage pro-inflammatory
dc.description.none.fl_txt_mv 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.
Instituto de Estudios Inmunológicos y Fisiopatológicos
description 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.
publishDate 2016
dc.date.none.fl_str_mv 2016
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/85969
url http://sedici.unlp.edu.ar/handle/10915/85969
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/1932-6203
info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0164098
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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