Alcoholic patients have dysregulated peripheral immune responses, are more susceptible to bacterial or viral infections, and exhibit signs of inflammation in several organs, including lung, liver, and the brain (Cook, 1998). Peripheral innate immune dysregulation is central to the pathogenesis of alcoholic steatohepatitis (ASH) and alcoholic liver disease (ALD), which are both marked by inflammation (Keshavarzian et al., 2009; Mutlu et al., 2009). Alcohol ingestion increases gut permeability to macromolecules, also referred to as “gut leakiness”, allowing translocation of bacterial toxins through the intestines into the bloodstream (Leclercq et al., 2012, 2014b; Parlesak et al., 2000). Increased levels of plasma endotoxins then activate immune responses in peripheral organs. Gut permeability can be increased for up to 2 weeks after cessation of alcohol consumption (Bjarnason et al., 1984). Even in healthy individuals, binge-drinking alcohol increases serum levels of gut-derived bacterial products such as LPS and 16S DNA, activating innate immune signaling and increasing circulating cytokines like TNF-α and IL-6 (Bala et al., 2014; Leclercq et al., 2012). In individuals with an alcohol use disorder, however, endotoxin levels increase > 5-fold compared
