Journal
PLOS ONE
Volume 11, Issue 11, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0163694
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Funding
- Agencia Nacional de Promocion Cientifica y Tecnologica (ANPCYT)
- INSERM, CNRS, Institut Pasteur de Lille, Universite de Lille
- CONICET-DAAD
- Argentinian Ministry of Science, Technology and Innovation
- French Ministry for Research and Higher Education [EGOS A12803]
- CONICET
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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.
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