NLRP3 is an intracellular protein complex composed of NLRP3, ASC, and pro-caspase-1, and it serves as a platform to activate pro-inflammatory cytokines IL-1β and IL-18 (Schroder et al., 2010). Recent structural studies have revealed the importance of ASCPYD/ASCPYD and NLRP3PYD/ASCPYD interactions during inflammasome activation (Lu et al., 2014). NLRP3 can be activated by pathogens and by a wide range of cytosolic DAMPs, including ATP, potassium efflux, alum, uric acid crystals and amyloid β (Jin and Flavell, 2010; Schroder et al., 2010) and is also involved in the pathogenesis of metabolic diseases, brain disorders, such as Alzheimer’s disease (Heneka et al., 2013), autoimmune encephalomyelitis (EAE), and it also contributes to ethanol-induced neuroinflammation in the cerebellum of ethanol-treated mice (Lippai et al., 2013). Although the cellular and molecular mechanisms of ethanol-induced inflammasome activation in the brain remain to be defined, we herein provide evidence that cultured astrocytes express NLRP3 and are capable of promoting ASC oligomerization to allow the recruitment of NLRP3 and caspase-1 activation (Lu et al., 2014) along with the production of IL-1β and IL-18 in response to ethanol, ATP
