Both infiltrating macrophages (IMs) and microglia become activated in response to tissue damage and can release proinflammatory cytokines, which may contribute to neuroinflammation and blood-brain barrier breakdown [8, 9]. Further, microglia, a resident macrophage of the CNS, become activated in the brain after alcohol use [8, 9]. In addition to microglia, peripheral macrophages can be recruited into the CNS under pathologic conditions and may serve to amplify ongoing neuroinflammation [10]. Recent evidence suggests that breakdown of the blood-brain barrier occurs in postmortem tissue of AUD patients, and knockout of Toll-like receptor 4 (TLR4), an important innate immune signaling receptor expressed by microglia and peripheral macrophages, protects from the ensuing alcohol-induced neuroinflammation [11]. While microglial activation has been studied in alcohol-induced neuroinflammation, the potential infiltration of peripherally recruited macrophages is yet to be evaluated.
