DescriptionBRUCELLA-INFECTED CELLS DISPLAY A FRAGMENTED MITOCHONDRIAL POPULATION THAT DOES NOT CHANGE CELL SENSITIVITY TO TNF-INDUCED APOPTOSIS
ARNOULD Thierry1, LOBET Elodie1, WILLEMART Kevin2, NINANE Noelle1, DEMAZY Catherine1, SEDZICKI Jaroslaw3, LELUBRE Christophe4, DE BOLLE Xavier2, RENARD Patricia1, RAES Martine1, DEHIO Christoph3, LETESSON, Jean-Jacques2
1. URBC -NARILIS, University of Namur (UNamur), Belgium
2. URBM -NARILIS (University of Namur (UNamur), Belgium
3. Biozentrum, University of Basel, Switzerland
4. Laboratory of Experimental Medicine (ULB 222 Unit), ULB, Belgium
Introduction: 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.
Material and 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.
Conclusion: This study brings new information regarding host-pathogen relationship and cross talk between Brucella and mitochondria in infected cells.
|Period||23 Oct 2018 → 25 Oct 2018|
9th World Congress on Targeting Mitochondria
|Degree of Recognition||International|