Modulating Role of Alcohol and Acetaldehyde on Neutrophil and Monocyte Functions In Vitro

Abstract

Moderate alcohol intake lowers coronary heart disease risk. Because polymorphonuclear neutrophils (PMN) and monocytes (Mo) play a role in atherosclerotic plaque destabilization we investigated in vitro effects of clinically relevant concentrations of ethanol (0.05, 0.125, 0.25, and 0.5%) and its metabolite acetaldehyde (0.0625, 0.125, and 0.5 mM) on human PMN and Mo phagocytic functions. PMN and Mo from healthy volunteers were separated and purified according standard methods and the following parameters were determined: phagocytic activity (percent of phagocytes with at least one ingested particle), ingestion index (number of ingested particles per 100 phagocytic cells), and intracellular killing (percent of dead ingested particles per 100 phagocytes) using acridine orange method and living yeast cells as targets. Reactive oxygen species (ROS) formation of ethanol-treated PMN and Mo was evaluated using 2,7-dichlorofluorescin method and results were expressed as percent of fluorescence-positive cells. Ethanol and acetaldehyde significantly reduced PMN phagocytic functions, with the exception of phagocytic activity, starting at 0.125% for ethanol and 0.0625 mM for acetaldehyde. Mo ingestion and microbicidity were decreased at ethanol concentrations of 0.5% without effect on Mo phagocytic activity. Acetaldehyde impaired Mo ingestion ability starting at 0.0625 mM and phagocytic activity at 0.5 mM while was without effect on Mo microbicidity. ROS production was significantly increased at ethanol concentrations 0.25 and 0.5% in PMN and at 0.5% in Mo. These results might partly explain the beneficial role of moderate use of alcohol on cardiovascular disease.