Ethanol directly activates microglia in vitro to increase expression of mRNAs coding for TNF-α, IL-1β, and iNOS (Fernandez-Lizarbe et al., 2009). Increases in microglial markers (i.e., IBA1 or CD11B) are also observed in mouse brain following binge or chronic ethanol drinking and in human postmortem brain from alcoholics (Alfonso-Loeches et al., 2010; Barton et al., 2017; He and Crews, 2008; Qin and Crews, 2012b; Rubio-Araiz et al., 2016; Walter et al., 2017; Zhao et al., 2013). Immunohistochemistry and transcriptome studies show upregulation of mRNA for TSPO (the 18 kDa translocator protein that is upregulated in activated microglia) in human alcoholic brain (Ponomarev et al., 2012). Methods for live in vivo imaging using PET labeling of TSPO have been developed (Vivash and OBrien, 2016), and reveal activated glia in alcohol-exposed adolescent baboons (Saba et al., 2017). However, PET labeling of TSPO in humans show fewer activated microglia in alcohol-dependent subjects compared with age-matched healthy controls (Hillmer et al., 2017). Cultured monocytes from these alcohol-dependent individuals also indicate blunted pro-inflammatory responses following an LPS challenge. Similarly, alcohol-dependent patients who had undergone recent
