Infections and tissue injuries can trigger an inflammatory reaction as a physiological host defence mechanism but in addition, cellular stress can also alert the immune system and induce adaptive responses. This kind of inflammation was termed “para-inflammation” by Medzhitov [24]. Recent studies have revealed that NLRP3 is the major receptor for endogenous danger insults to facilitate inflammatory responses. Petrilli et al. [25] demonstrated that the efflux of potassium, an effect evoked by many noxious stimuli, could activate NLRP3 inflammasomes. After this initial observation, several different activation mechanisms have been identified but still there is an ongoing debate about whether they are physiological inducers and what kind of responses they stimulate. The increased level of reactive oxygen species (ROS) induced by oxidative stress was one of the first stimuli which was demonstrated to trigger NLRP3 activation and promote CASP-1-dependent IL-1β secretion [26,27]. Furthermore, several studies have indicated that the release of cathepsin B after lysosomal damage can activate NLRP3 [28,29]. Lysosomal destabilization is also associated with the NLRP3 activation induced by cholesterol crystals in macrophages [30], probably involved in the inflammation
