Recently, Zhou et al. [37] demonstrated that mitochondria were crucially involved in the activation of NLRP3. They observed that increased mitochondrial production of ROS stimulated NLRP3 whereas the inhibition of ROS production, either with an enhanced autophagic uptake of damaged mitochondria or by inhibiting the expression of voltage-dependent anion channels (VDAC2), significantly suppressed the stimulation of NLRP3. Their study emphasized the significant role of mitochondria and in particular, their proper clearance by autophagy in the regulation of NLRP3 activation. Autophagy was also shown to be a fundamental host defence mechanism against invading intracellular microbes [38]. Moreover, deficiency in autophagy, e.g. in Crohn×s disease, triggers inflammatory responses and leads to tissue injuries [39]. It seems plausible that autophagy, a guardian of cellular sanctity, is a potent anti-inflammatory mechanism which controls the activation of danger sensors, i.e. NLRP3 inflammasomes (Figure 1).
