Additionally, recent evidence suggests that, in the developing brain, mice deficient in either CCL2 or CCR2 are protected from alcohol-induced neuroinflammation (including proinflammatory cytokine expression and microglial activation) and neurotoxicity when treated with an acute alcohol exposure at postnatal day 4 [29]. These results agree with the present data, which importantly is from adult mice with chronic alcohol consumption and provide further evidence for the importance of CCL2/CCR2 signaling in alcohol-induced neuroinflammation. Further experiments, including using CCL2 and CCR2 knockout adult mice under chronic alcohol conditions will also be informative.
