TY  - JOUR
A1  - Errea, Agustina
A1  - Cayet, Delphine
A1  - Marchetti, Philippe
A1  - Tang, Cong
A1  - Kluza, Jerome
A1  - Offermanns, Stefan
A1  - Sirard, Jean-Claude
A1  - Rumbo, Martin
T1  - Lactate inhibits the pro-inflammatory response and metabolic reprogramming in murine macrophages in a GPR81-independent manner
T2  - PLoS One
N2  - 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.
Y1  - 2016
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/41996
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-419969
UR  - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5112849
SN  - 1932-6203
N1  - Copyright: © 2016 Errea et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
VL  - 11
IS  - (11): e0163694
SP  - 1
EP  - 11
PB  - PLoS
CY  - Lawrence, Kan.
ER  -