DescriptionIntroduction: Mitochondria integrate a plethora of functions within a single organelle makes mitochondria a very attractive target to manipulate for intracellular pathogens. We characterized the crosstalk that exists between Brucella abortus, the causative agent of brucellosis, and the mitochondria of infected cells.
Methods: Cells were infected with Brucella (MOI: 300) for various post infection time and mitochondria population was analyzed after staining with Mitotracker Green. The abundance of fusion and fission markers was also analyzed by Western blot. In addition, Brucella replication in was assessed by CFU (Colony Forming Unit) in cells with fragmented mitochondria. Eventually, apoptosis of host cells infected or not was analyzed by active caspase-3 detection.
Results: We demonstrated that Brucella induce a drastic mitochondrial fragmentation at 48 hours post-infection. This fragmentation is DRP1-independent and might be caused by a deficit of mitochondrial fusion. However, mitochondrial fragmentation does not change Brucella replication efficiency or the susceptibility of infected cells to TNFα-induced apoptosis .
Conclusions: This study brings new information regarding host-pathogen relationship and cross talk between Brucella and mitochondria in infected cells.
 Lobet et al. (2018) Mitochondrial fragmentation affects neither the sensitivity to TNFα-induced apoptosis of Brucella-infected cells nor the intracellular replication of the bacteria. Sci. Rep. 8(1):5173
|Period||18 Sept 2018 → 21 Sept 2018|
|Event title||MiP : 13th International Meeting of Mitochondrial Physiology and Pathology: MitoEAGLE-Cost Action|
|Degree of Recognition||International|