dc.creatorErrea, Agustina Juliana
dc.creatorCayet, Delphine
dc.creatorMarchetti, Philippe
dc.creatorTang, Cong
dc.creatorKluza, Jerome
dc.creatorOffermanns, Stefan
dc.creatorSirard, Jean-Claude
dc.creatorRumbo, Martín
dc.date2016
dc.date2019-11-22T17:37:40Z
dc.date.accessioned2023-07-14T17:24:58Z
dc.date.available2023-07-14T17:24:58Z
dc.identifierhttp://sedici.unlp.edu.ar/handle/10915/85969
dc.identifierissn:1932-6203
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/7427401
dc.descriptionLactate 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.
dc.descriptionInstituto de Estudios Inmunológicos y Fisiopatológicos
dc.formatapplication/pdf
dc.languageen
dc.rightshttp://creativecommons.org/licenses/by/4.0/
dc.rightsCreative Commons Attribution 4.0 International (CC BY 4.0)
dc.subjectCiencias Médicas
dc.subjectLactate
dc.subjectGPR81
dc.subjectMacrophage pro-inflammatory
dc.titleLactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner
dc.typeArticulo
dc.typeArticulo


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