Mitochondrial dynamics during Legionella infection

The integration of diverse and important functions in a single organelle, such as production of ATP via oxidative phosphorylation, regulation of programmed cell death and generation of immune responses, makes mitochondria a very attractive structure to be targeted and modulated by bacterial pathogens. Legionella pneumophila is a Gram-negative bacterium and the causative agent of Legionnaires’ disease. The establishment of the Legionella-containing vacuole (LCV) within the host cytoplasm requires the remodeling of the LCV surface and the hijacking of endoplasmic reticulum vesicles, ribosomes and mitochondria during macrophage infection. Mitochondria association to the LCV was reported to be dependent on a type 4B secretion system (T4BSS) that translocates more than 300 bacterial effectors to the host cytoplasm during L. pneumophila infection. In order to shed light on the dynamics of this process, we developed a High Content Analysis of mitochondrial trafficking using confocal images acquired during GFP-tagged Legionella infection of human primary macrophages. Our results indicate that L. pneumophila establishes stochastic contacts with host mitochondria during the first 6h of infection in a T4BSS-independent manner while it promotes T4BSS-dependent changes in the mitochondrial networks.