About
We previously showed that the intracellular bacterium Legionella pneumophila, the causative agent of Legionaries’ disease in humans, alters mitochondrial morphology by injecting the effector MitF in the host cell through its type IV secretion system (T4SS), and therefore reduces mitochondrial respiration of infected human macrophages. As the ultrastructure of mitochondria is determinant for their respiratory activity, we hypothesized that alterations of the respiratory status of infected cells are caused by the reconfiguration of the mitochondrial Electron Transport Chain (ETC) complexes during infection. This project aimed to determine the putative role of ETC complexes during bacterial infection and explored the possibility of targeting them to tackle bacterial infection, as a host-directed therapy approach