Previously, we and others have shown that proinflammatory cytokine expression is increased in the brain after chronic alcohol exposure [12, 13, 22]. Because of the proinflammatory environment in the CNS induced by alcohol consumption, we hypothesized that macrophages may have altered the expression of surface activation markers. Using flow cytometry of isolated CNS immune cells from the total brain, we observed that alcohol modestly altered the expression of multiple investigated activation markers of the CD11b+CD45hi macrophages, including CD86, CD68, MHC-II, CD163, and CD206 (Fig. 3d). The expression of these markers was not significantly changed on CNS IMs, although an increasing trend was observed for CD86 and a decreasing trend for CD163. CVC treatment did not significantly alter the expression of these markers on CD11b+CD45hi macrophages (Fig. 3d), suggesting that the activation state of IMs in the CNS in alcohol-fed mice is independent of CCR2/5 signaling.
