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Fig. 2. It is critical to maintain the balance between mitophagy and inflammasome complex activation to promote host defense while controlling excessive pathological inflammation during infection. Among pathogen products, HIV ssRNA, gp120, and Tat can activate the NLRP3 inflammasome through inhibition of mitophagy and mitochondrial damage. In addition, Pseudomonas aeruginosa activates the NLRC4 inflammasome through increased ROS production and release of mtDNA. Mechanistically, SESN2 and Parkin participate in the suppression of NLRP3 inflammasome activation through mitophagy induction. Several pathogens including HCV can also increase mitochondrial ROS production, resulting in pathological responses during infection and inflammation. In a sepsis model, mitophagy activation to control mitochondrial ROS was found to be related to enhanced host defense.
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