Mitochondria have a crucial role in the regulation of innate immunity responses [54,55]. In addition to the ROS-dependent activation of NLRP3 inflammasomes, mitochondria (i) are involved in the control of antiviral RIG-1-like receptor (RLR) signaling pathways, (ii) contain NLRX1 receptors which monitor e.g. ROS production, and (iii) secrete several DAMPs, such as ROS, mitochondrial DNA (mtDNA) and formyl peptides [54,56]. The studies by Zhou et al. [37] and Nakahira et al. [57] clearly demonstrated that secretion of ROS and mtDNA from mitochondria activated inflammasomes, i.e. mitochondria with disrupted integrity and impaired autophagic clearance are the crucial regulators of inflammasomal activation and subsequently inflammatory responses. Nakahira et al. [57] revealed that depletion of autophagic proteins impaired mitochondrial integrity and increased their ROS production. They also demonstrated that ROS were required for caspase-1 activation, a prerequisite for the maturation of IL-1β and IL-18. They also observed that NLRP3 mediates the release of mtDNA which seems to function as a co-activator of caspase-1. In contrast, Zhou et al. [27] reported that ROS could dissociate the complex between thioredoxin (TRX) and thioredoxin-interacting protein (TXNIP),
