Difference between revisions of "Arnould 2018 MiP2018a"
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{{Abstract | {{Abstract | ||
|title=[[Image:MiPsocietyLOGO.JPG|left|90px|Mitochondrial Physiology Society|MiPsociety]] Brucella-infected cells display a fragmentation of mitochondrial population: mechanisms and putative functional impact. | |title=[[Image:MiPsocietyLOGO.JPG|left|90px|Mitochondrial Physiology Society|MiPsociety]] ''Brucella''-infected cells display a fragmentation of mitochondrial population: mechanisms and putative functional impact. | ||
|info=[[MiP2018]] | |info=[[MiP2018]] | ||
|authors=Arnould T, Lobet E, Willemart K, Ninane N, Demazy C, Sedzicki J, Lelubre C, De Bolle X, Renard P, Raes M, Dehio C, Letesson JJ | |authors=Arnould T, Lobet E, Willemart K, Ninane N, Demazy C, Sedzicki J, Lelubre C, De Bolle X, Renard P, Raes M, Dehio C, Letesson JJ | ||
|year=2018 | |year=2018 | ||
|event=MiP2018 | |event=MiP2018 | ||
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action | |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]] | ||
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. | 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. | ||
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. | 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. | ||
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]. | 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]. | ||
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}} | }} | ||
{{Labeling | {{Labeling | ||
|area=mt-Medicine | |area=mt-Structure;fission;fusion, mt-Medicine | ||
|diseases=Infectious | |diseases=Infectious | ||
|organism=Human | |organism=Human | ||
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Arnould T(1), Lobet E(1), Willemart K(2), Ninane N(1), Demazy C(1), Sedzicki J(3), Lelubre C(4), De Bolle X(2), Renard P(1), Raes M(1), Dehio C(3), Letesson JJ(2) | Arnould T(1), Lobet E(1), Willemart K(2), Ninane N(1), Demazy C(1), Sedzicki J(3), Lelubre C(4), De Bolle X(2), Renard P(1), Raes M(1), Dehio C(3), Letesson JJ(2) | ||
::::#URBC -NARILIS | ::::#URBC -NARILIS | ||
::::#URBM -NARILIS, | ::::#URBM -NARILIS, Univ Namur (UNamur); Belgium | ||
::::#Biozentrum, Univ | ::::#Biozentrum, Univ Basel, Switzerland | ||
::::#Lab Experimental Medicine (ULB 222 Unit), ULB, Belgium. - [email protected] | ::::#Lab Experimental Medicine (ULB 222 Unit), ULB, Belgium. - [email protected] | ||
| Line 42: | Line 42: | ||
== References == | == References == | ||
#Lobet E, Willemart K, Ninane N, Demazy C, Sedzicki J, Lelubre C, De Bolle X, Renard P, Raes M, Dehio C, Letesson JJ, Arnould T (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 | #Lobet E, Willemart K, Ninane N, Demazy C, Sedzicki J, Lelubre C, De Bolle X, Renard P, Raes M, Dehio C, Letesson JJ, Arnould T (2018) Mitochondrial fragmentation affects neither the sensitivity to TNFα-induced apoptosis of Brucella-infected cells nor the intracellular replication of the bacteria. Sci Rep 8:5173. | ||
Latest revision as of 08:00, 13 September 2018
 |
Link: MiP2018
Arnould T, Lobet E, Willemart K, Ninane N, Demazy C, Sedzicki J, Lelubre C, De Bolle X, Renard P, Raes M, Dehio C, Letesson JJ (2018)
Event: MiP2018
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.
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.
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].
This study brings new information regarding host-pathogen relationship and cross talk between Brucella and mitochondria in infected cells.
• Bioblast editor: Plangger M, Kandolf G
Labels: MiParea: mt-Structure;fission;fusion, mt-Medicine Pathology: Infectious
Organism: Human Tissue;cell: HeLa
Affiliations
Arnould T(1), Lobet E(1), Willemart K(2), Ninane N(1), Demazy C(1), Sedzicki J(3), Lelubre C(4), De Bolle X(2), Renard P(1), Raes M(1), Dehio C(3), Letesson JJ(2)
- URBC -NARILIS
- URBM -NARILIS, Univ Namur (UNamur); Belgium
- Biozentrum, Univ Basel, Switzerland
- Lab Experimental Medicine (ULB 222 Unit), ULB, Belgium. - [email protected]
Figure 1
Figure 1. Brucella abortus infection induces mitochondrial fragmentation in infected HeLa cells. TOM20 immunostaining in HeLa cells infected or not (control) with B. abortus 2308 mCherry - 48 h post-infection. Green: TOM20 (Alexa488)/Red: B. abortus 2308 (mCherry)/Turquoise: Nuclei (Hoechst)
References
- Lobet E, Willemart K, Ninane N, Demazy C, Sedzicki J, Lelubre C, De Bolle X, Renard P, Raes M, Dehio C, Letesson JJ, Arnould T (2018) Mitochondrial fragmentation affects neither the sensitivity to TNFα-induced apoptosis of Brucella-infected cells nor the intracellular replication of the bacteria. Sci Rep 8:5173.
