functionally links ER stress to the inflammasome and activation of NF-κB, was found to be 1.7 fold higher in the hippocampus of alcoholics (McClintick et al., 2013). Recently, neuroinflammation has been linked to alcoholism and may play a role in the addiction process (Crews et al., 2011; Mayfield et al., 2013). It has been hypothesized that lipopolysaccharides (LPS) introduced into circulation from the gut may be responsible for neuroinflammation (Mayfield et al., 2013) by activating peripheral TLR4 receptors to produce circulating cytokines that can cross the blood-brain barrier. Others have shown that a robust inflammatory response to ethanol does not require lipopolysaccharides from the gut-liver axis, and that a direct effect of ethanol on Toll-like receptor 4 can initiate neuroinflammation (Fernandez-Lizarbe et al., 2013). Our data show that a 24 h exposure to ethanol was sufficient to initiate this inflammatory response in LCLs without exposure to LPS.
