dc.creator | Errea, Agustina Juliana | |
dc.creator | Cayet, Delphine | |
dc.creator | Marchetti, Philippe | |
dc.creator | Tang, Cong | |
dc.creator | Kluza, Jerome | |
dc.creator | Offermanns, Stefan | |
dc.creator | Sirard, Jean-Claude | |
dc.creator | Rumbo, Martín | |
dc.date | 2016 | |
dc.date | 2019-11-22T17:37:40Z | |
dc.date.accessioned | 2023-07-14T17:24:58Z | |
dc.date.available | 2023-07-14T17:24:58Z | |
dc.identifier | http://sedici.unlp.edu.ar/handle/10915/85969 | |
dc.identifier | issn:1932-6203 | |
dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/7427401 | |
dc.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. | |
dc.description | Instituto de Estudios Inmunológicos y Fisiopatológicos | |
dc.format | application/pdf | |
dc.language | en | |
dc.rights | http://creativecommons.org/licenses/by/4.0/ | |
dc.rights | Creative Commons Attribution 4.0 International (CC BY 4.0) | |
dc.subject | Ciencias Médicas | |
dc.subject | Lactate | |
dc.subject | GPR81 | |
dc.subject | Macrophage pro-inflammatory | |
dc.title | Lactate inhibits the pro-inflammatory response and metabolic reprogramming in Murine macrophages in a GPR81-independent manner | |
dc.type | Articulo | |
dc.type | Articulo | |