Chronic alcohol exposure induces a complex, multi-organ response with activation of a variety of immune responses and inflammatory expression. Previous research has sought to characterize the gene expression changes caused by chronic alcohol in various parts of the brain. Gene expression analyses in humans [36–39] and rodents [40] reveal alterations in genes related to neurons and neurogenesis, axonal growth, myelin regulation, intracellular signaling, protein trafficking, and other critical cell processes. Interestingly, neuroimmune genes were significantly increased in the frontal cortex of human patients with alcohol use disorder [38], while PET studies using markers of glial density have revealed that alcohol reduces or alters the behavior of CNS glia, likely representing changes in the local neuroimmune milieu [41–43]. Using a targeted screen, we observed alterations in inflammation-related transcripts in the CNS after chronic alcohol in mice and expanded our focus to investigate the hippocampus, cortex, and cerebellum. We observed the upregulation of multiple proinflammatory genes similar to previous descriptions, and some of these were altered by the treatment of CVC to block CCR2/5 signaling. As noted previously, some cytokine expression is
