RésuméBrucellosis is one of the most common worldwide zoonosis caused by a facultative intracellular gram negative coccobacilli of the genus Brucella. It affects a wide range of mammals and induces abortion and sterility causing huge economic issue. Brucella is a furtive bacteria generating a chronic disease if not treated. At this time, no treatment nor safe or effective human vaccines exist. In this master thesis, we demonstrated that Brucela melitensis persists in a CD1 1c* reservoir
cells able to resist to protective memory response in wild type C57B/6 mice. Surprisingly, the co-infection by the parasite Trypanosoma brucei appears able to increase the immune control of chronic Brucella infection. Following co-infection, the mice become able to eliminate Bruce/la thanks to a CD4* T cells dependent Th 1 immune response, as demonstrated by using IL-12 and IFNy deficient mice. This mechanism is not antigen specific as T. brucei coinfection is also able to favor the elimination of B. suis and B. abortus and that T. cruzi coinfection display a similar effect on B. melitensis. Another central point of this work was to characterized Brucella's dissemination following several route of infection. We highlighted the fact that the route of dissemination affects the dissemination and could thus affects the pathology of brucellosis.
|la date de réponse||2017|
|Superviseur||Eric MURAILLE (Promoteur) & JEAN-JACQUES LETESSON (Promoteur)|