NOD-like receptors family members, NLRP1, NLRP3, NLRC4, and AIM2 (a member of the PYHIN protein family), have been identified as being capable of forming inflammasomes, multiprotein complexes that activate caspase-1, which leads to the processing and secretion of pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18. Among NLRs, NLRP3 is currently the most fully described inflammasome. It consists of the NLRP3 scaffold, adaptor ASC (apoptosis-associated speck-like protein containing a CARD) and caspase-1. Nevertheless, the molecular and cellular mechanisms of NLRP3 activation remain unclear. Different mechanisms have been postulated, such as lysosomal damage (Hornung and Latz, 2010), potassium leakage (Arlehamn et al., 2010), and reactive oxygen species (ROS) formation (Schroder et al., 2010; Shimada et al., 2012a). Recent studies support the role of mitochondrial adaptors (Subramanian et al., 2013), mitochondria calcium fluxes (Triantafilou et al., 2013) and ROS formation (Zhou et al., 2011; Shimada et al., 2012b) in inflammasome activation.
