Alcohol-Induced miR-27a Regulates Differentiation and M2 Macrophage Polarization of Normal Human Monocytes

摘要: Alcohol abuse is a leading cause of liver disease characterized by inflammation, fatty liver, alcoholic hepatitis, or cirrhosis. Immunomodulatory effects alcohol on monocytes and macrophages contribute to disease. use, an independent risk factor for progression hepatitis C virus (HCV) infection-mediated disease, impairs host defense alters cytokine production monocyte/macrophage activation. We hypothesized that HCV have synergistic the phenotype function monocytes. Our data show acute binge drinking in healthy volunteers results increased frequency CD16(+) CD68(+) M2-type (CD206(+), dendritic cell [DC]-SIGN(+)-expressing IL-10-secreting) circulating CD14(+) Expression HCV-induced CD68 M2 markers (CD206 DC-SIGN) normal was further enhanced presence alcohol. The levels microRNA (miR)-27a significantly upregulated cultured as compared with alone. functional role miR-27a macrophage polarization demonstrated transfecting inhibitor resulted reduced alcohol- HCV- mediated monocyte activation (CD14 expression), DC-SIGN IL-10 secretion. Overexpression secretion via ERK signaling pathway. found promoted phosphorylation downregulating expression sprouty2 Thus, we identified target human In summary, our study demonstrates regulatory alcohol-induced polarization.