We hypothesized that, because the chemokine CCL2 is highly expressed in human and mouse brains after chronic alcohol use, chronic ethanol promotes infiltration of peripheral IM recruitment in the brain, those IMs contribute to ethanol-induced neuroinflammation, and treatment with CVC to inhibit infiltration of peripheral macrophages will protect from proinflammatory signaling in the CNS. Here, we present evidence of region-specific peripheral macrophage recruitment, associated with cytokine expression and microglial activation after exposure to a model of chronic alcohol in mice. Treatment with CVC reduced the number of IMs in the CNS, reduced cytokine expression, and corrected microglial morphology.
