Figure 2 .

Interplay between autophagy and inflammasome activation during bacterial infection. Extracellular inject virulence factors into host cells via T3SS. Some of the virulence factors activate NLRC4 mediated by NAIP proteins, and other virulence factors have strong destructive power to mitochondria. The damaged mitochondria release mtDNA, cardiolipin, ROS, and other activators of AIM2 and NLRP3. Then, AIM2, NLRP3, Caspase-11 and NLPC4 combine with caspase-1 to form inflammasomes. Activated inflammasomes cleave proteins that are important for autophagy progress, such as ATG16L1, TRIF, and other receptor proteins, and trigger pyroptosis and liberate a number of inflammatory factors. However, activated autophagy during bacterial infection will attenuate pyroptosis and clear defective mitochondria which leads to the downregulation of such activators as mtDNA, cardiolipin, ROS, and Ca²⁺ of inflammasomes. Autophagy can also swallow proIL-18 and IL-1β which are necessary for mature inflammatory factors. NLRC4, NLR family CARD domain-containing protein 4; NLRP3, NACHT, LRR and PYD domains-containing protein 3; AIM2, absent in melanoma 2; mtDNA, mitochondria DNA; ROS, Reactive oxygen species.