Cell death is ultimately caused by cellular innate immune response elicited by the inflammasome activation. We show that the activation of NLRP3 by either ATP, LPS or ethanol mainly triggers pyroptosis a caspase-1-dependent inflammatory form of programmed cells in which dying cells release their cytoplasmic content, including cytokines, into the extracellular space. Nevertheless, ethanol or ATP by inducing mitochondrial stress and mROS production, can also trigger apoptosis by activating Apaf-1, caspase-9, and caspase-3, and the apoptosome complex (Morizot, 2012). It is noteworthy that inflammasomes and apoptosomes are two mechanisms of the immune cells by which compromised cells are eliminated and share many similarities in their regulatory response to cellular stress (Latz et al., 2013). Yet whether these two mechanisms act independently or are linked, and whether their individual contributions depend on the intensity and type of cell stimuli (e.g., bacteria, virus, DAMPs; Doitsh et al., 2014), are uncertain (Latz et al., 2013). Nevertheless, in vivo evidence from the immunohistochemical data reported herein (Figure 1) and our previous studies support the in vitro finding since we observed that chronic ethanol treatment
