Interestingly, we observed the most pronounced alterations in the surface activation markers between microglia of alcohol-fed mice and microglia from mice treated with CVC. It is important to note that for flow cytometric analysis for surface marker expression, we used total brain microglia and infiltrating macrophages, whereas other assays (such as histology and biochemical measurements) used more localized populations or tissues for analysis. Therefore, cell surface marker analysis may not fully reflect the micromilieu within subregions of the brain. A possible explanation for the alterations in microglial surface markers is that in the absence of IMs, the remaining microglia are forced to assume a more activated phenotype and respond to the damage induced by alcohol. Interestingly, while we observed surface protein activation markers in microglia, we also observed an activated morphologic phenotype with increased soma size and reduced microglial cell process length. For this analysis, we focused on microglia in the hippocampus, the site of significant peripheral macrophage infiltration (Fig. 2c) and an increase in protein and mRNA expression of proinflammatory cytokines (Fig. 4). Microglial morphology is one indicator of
