Inflammation plays critical roles in the pathogenesis of multiple disorders of the central nervous system (CNS; Weiner and Selkoe, 2002; Hunot and Hirsch, 2003) and has recently been implicated as a mechanism of alcoholism-induced neuropathology (Crews et al., 2011; Kelley and Dantzer, 2011; Yakovleva et al., 2011). An important player eliciting activation of immune functions in the CNS in response to alcohol is Toll-like receptor (TLR) 4, which contributes to ethanol-induced activation of nuclear factor kappa B (NFκB) and consequently activates transcription of pro-inflammatory chemokines, cytokines, oxidases, and proteases. TLRs have well-established roles in pathogen detection and initiation of an innate immune response that consequently specifies adaptive responses during infection (O’Neill, 2006).
