Although the CNS was long considered an immune-privileged compartment, an appreciation for peripheral immune infiltration in the setting of diseases has been accepted. Only recently has infiltration of peripheral macrophages been described in the setting of alcohol-induced neuroinflammation [11, 22]. Using a different alcohol model than previously studied in mice, we confirm this observation using flow cytometry of total immune cells in the brain, detecting an increase in CD11b+CD45hi macrophages. Peripheral macrophages have previously been distinguished from microglia (CD11b+CD45lo), and although expression of CD45 can shift during inflammation, gene expression studies suggest its expression level remains a distinguishing feature between the two cell types [25]. Additionally, we created CX3CR1eGFP/+ CCR2RFP/+ mice to allow for visualization and localization of infiltrating CCR2+ macrophages. While we observed a trend toward increased macrophages in the cortex and cerebellum, the largest alcohol-induced increase observed was in the hippocampus, a region of significant alcohol-related inflammation in both rodents and humans [8, 26, 27]. These data suggest that alcohol-induced macrophage infiltration into the CNS may be region-specific and possibly linked to localized neural damage and immune signaling.
