Ethanol is known to act as a powerful epigenetic disruptor and is potentially able to interfere with cellular metabolism and differentiation. In particular, neuroinflammation and oxidative damage of mitochondria and cellular proteins are thought to contribute to the progression of neurological disorders initiated by alcohol abuse [4]. Ethanol can initiate an innate immune-like response in the CNS [5] via two main receptors and their respective signaling pathways: the membrane bound toll-like receptors (TLRs) [6] and the cytoplasmic NOD-like receptor family, pyrin domain containing 3 (NLRP3). NLRP3 forms intracellular danger-sensing multi-protein platforms called inflammasomes [5]. Activation of both the TLR- and NLRP3-mediated pathways in mammals is correlated with aging [7, 8] and cellular insults, including ethanol exposure [5]. NLRP3 can activate inflammatory caspases, e.g. Caspase-1 (Casp1), which accelerates the aging process through the impairment of autophagy, thus eventually leading to cell death [9]. On the other hand, ethanol has also been shown to induce the activation of Caspase-3 (Casp3)-dependent apoptosis and necrosis in vivo [10]. However, whether ethanol exposure activates these cellular inflammatory pathways in human cells is not clear.
