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- Arnould 2018 MiP2018a + ([[Image:MITOEAGLE-logo.jpg|left|100px|link … [[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]]</br>Mitochondria integrate a plethora of functions within a single organelle, which 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. </br></br>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 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.</br></br>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 [1].</br></br>This study brings new information regarding host-pathogen relationship and cross talk between ''Brucella'' and mitochondria in infected cells.ella'' and mitochondria in infected cells.)
