Ethanol (<scp>E</scp>t<scp>OH</scp>)‐Induced <scp>TGF</scp>‐β₁ and Reactive Oxygen Species Production Are Necessary for <scp>E</scp>t<scp>OH</scp>‐Induced Alveolar Macrophage Dysfunction and Induction of Alternative Activation

Abstract

EtOH treatment increased oxidant stress, TGF-β(1) production, and alternative activation in NR8383 cells. However, GSH supplementation and ablation of TGF-β(1) signaling prevented these effects. This suggested that the EtOH-induced switch to an M2 phenotype was a result of decreased antioxidant availability and increased TGF-β(1) signaling. Preventing EtOH-induced induction of alternative activation may improve alveolar macrophage function in alcoholic subjects and decrease the risk of respiratory infections.