may be more sensitive to ethanol-induced neuroimmune responses (Alfonso-Loeches et al., 2013; Bala et al., 2014; Barton et al., 2017; Baxter-Potter et al., 2017; Pascual et al., 2017; Wilhelm et al., 2015). Age is also a factor in susceptibility to alcohol-induced neuroinflammation (Kane et al., 2014). Depending on the brain region, ethanol withdrawal is associated with increased mRNA expression of cytokines and is mediated by release of corticotropin releasing factor and HMGB1 (Knapp et al., 2016; Whitman et al., 2013). In addition, ethanol exposure can potentiate neuroimmune activation caused by systemic administration of other inflammatory agents, such as LPS and the TLR3 agonist polyI:C (Qin and Crews, 2012a; Qin et al., 2008).
