Lactate Inhibits the Pro-Inflammatory Response and Metabolic Reprogramming in Murine Macrophages in a GPR81-Independent Manner.

Agustina Errea 1, 2 Delphine Cayet 3 Philippe Marchetti 4 Cong Tang 5 Jerome Kluza 4 Stefan Offermanns 5 Jean-Claude Sirard 3 Martin Rumbo 1, 2
1 UNLP - Universidad Nacional de la Plata [Argentine]
2 Instituto de Estudios Inmunológicos y Fisiopatológicos
3 CIIL - Centre d’Infection et d’Immunité de Lille (CIIL) - U1019 - UMR 8204
4 JPArc - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer (JPArc) - U1172
5 MPI-HLR - Max Planck Institute for Heart and Lung Research
Abstract : 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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PLoS ONE, Public Library of Science, 2016, 11 (11), pp.e0163694. 〈10.1371/journal.pone.0163694〉
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http://www.hal.inserm.fr/inserm-01529298
Contributeur : Jean-Claude Sirard <>
Soumis le : mardi 30 mai 2017 - 14:57:27
Dernière modification le : jeudi 20 septembre 2018 - 20:10:02

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Agustina Errea, Delphine Cayet, Philippe Marchetti, Cong Tang, Jerome Kluza, et al.. Lactate Inhibits the Pro-Inflammatory Response and Metabolic Reprogramming in Murine Macrophages in a GPR81-Independent Manner.. PLoS ONE, Public Library of Science, 2016, 11 (11), pp.e0163694. 〈10.1371/journal.pone.0163694〉. 〈inserm-01529298〉

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