2010, 2012). The present findings further support the role of TLR4 in ethanol-induced NLRP3 inflammasome activation and IL-1β and IL-18 production in glial cells, events that contribute to ethanol-induced neuroinflammation. To support our results, a recent study has demonstrated that ethanol-impaired neurogenesis is associated with induction of IL-1β and with inflammasome NALP1 and NALP3 activation in both neurons and astrocytes, and that these events can be blocked with both the IL-1β receptor and antagonist rIL-1Ra (Zou and Crews, 2012). Similarly, the intracranial administration of IL-1Ra prevents alcohol-induced inflammasome activation and the up-regulation of IL-1β and TNF-α in the cerebellum of ethanol-treated mice (Lippai et al., 2013). These results indicate the importance of ethanol-induced inflammasome activation and IL-1β production in the neuroinflammatory effects of ethanol.
