Lactate induces alternative polarization (M2) of macrophages under lipopolysaccharide stimulation in vitro through G-protein coupled receptor 81

To the Editor:Sepsis is a life-threatening systemic inflammatory response syndrome caused by the host’s maladjusted immune response to infection.Hyperlactatemia is an important manifestation of severe sepsis.Initial hyperlactatemia is associated with increased mortality in sepsis.[1]Hyperlactatemia and immunosuppression often occur simultaneously in the late stage of sepsis.G-proteincoupled receptor 81(GPR81)is a cell-surface G-protein coupled receptor,which is activated by lactate.It has been reported that lactate inhibits the function of macrophages through GPR81,and alleviates liver injury in immune hepatitis.[2]In sepsis,alternative polarization(M2)of macrophages reduces the production of pro-inflammatory factors,weakens the phagocytosis of macrophages,and inhibits the immune response.GPR81 pathway is closely related to M2 polarization of macrophages.Therefore,we designed this experiment to explore the relationship between lactate and M2 of macrophages and further explored the relationship between this effect and the GPR81 pathway in sepsis.