Our results demonstrate that microglial phagocytosis of Aβ1–42 is significantly suppressed following 1-day exposure to 75 mM ethanol. This dose of ethanol is in the high range and is attained in human following binge drinking or in heavy drinkers. Similar doses have previously been used to study phagocytosis in vitro [33, 36]. Suppressive effects of alcohol on phagocytosis have previously been reported in studies examining macrophages (see [35] for review). Alcohol reduces uptake of Pseudomonas aeruginosa [36], and of Candida albicans [75], and inhibition can be seen as soon as 1 h after treatment with ethanol [76]. In contrast to macrophages, there are limited studies of the effects of alcohol exposure on microglial phagocytosis. In neonatal mice [77], acute binge-like alcohol exposure induced microglial activation and phagocytosis of damaged neurons, suggesting that acute ethanol exposure could be protective during early development. It was also shown using a similar acute exposure model, that although activated microglia were observed near to dead cells in the cortex, that apoptotic bodies accumulated, interpreted that the rate of cell death exceeded microglial clearance capacity [78].
