When mitophagy dictates the outcome of cellular infection: the case of Brucella abortus

Summary: The facultative intracellular pathogen Brucella abortus interacts with host cell organelles, particularly the mitochondria, for replication. This study demonstrates that B. abortus induces fragmentation of the mitochondrial network, mitophagy, and the formation of mitochondrial Brucella-containing vacuoles during late stages of cellular infection. This process is dependent on the expression of the mitophagy receptor BNIP3L, which is regulated by iron-dependent stabilization of hypoxia-inducible factor 1 alpha. BNIP3L-mediated mitophagy is advantageous for bacterial exit from the host cell. These findings highlight the intricate relationship between Brucella trafficking and the mitochondria during host cell infection.