Many genes associated with inflammatory responses, including interleukins and chemokines, were affected by ethanol (Table 2). These fell into many pathways (Supplemental Table S2). Pathways related to inflammation and neuroimmune activation showed increased overall expression in the alcohol-treated cells, including neuroinflammation signaling, Th1 and Th2 activation, NFκB, interleukin signaling, STAT3, JAKs in cytokine signaling, and T-cell receptors. Higher activation of neuroimmune pathways has been shown in post-mortem brain tissue from alcoholics (Crews, Qin, Sheedy, Vetreno, & Zou, 2013; McClintick et al., 2013) and in animal studies (Blednov et al., 2011; Qin et al., 2008). Chronic activation of neuroimmune pathways is one of the hallmarks of alcohol use disorders (Crews & Vetreno, 2016; Mayfield et al., 2013). Analyses of upstream regulators indicate that the observed changes in expression could be related to ethanol’s activation of Toll-like receptors, NFκB, and TNF. Lipopolysaccharide (LPS) was also listed as a putative regulator, although the LCLs were not exposed to LPS, indicating that the changes were similar to those seen when exposed to LPS, i.e. immune stimulation. In contrast to the 24 h study (McClintick
