Trypanosoma Infection Favors Brucella Elimination via IL-12/IFNγ-Dependent Pathways

This study develops an original co-infection model in mice using , the most frequent cause of human brucellosis, and , the agent of African trypanosomiasis. Although the immunosuppressive effects of in natural hosts and mice models are well established, we observed that the injection of in mice chronically infected with induces a drastic reduction in the number of in the spleen, the main reservoir of the infection. Similar results are obtained with - and -infected mice and -infected mice co-infected with , demonstrating that this phenomenon is not due to antigenic cross-reactivity. Comparison of co-infected wild-type and genetically deficient mice showed that elimination required functional IL-12p35/IFNγ signaling pathways and the presence of CD4 T cells. However, the impact of wild type and an attenuated mutant of on were similar, suggesting that a chronic intense inflammatory reaction is not required to eliminate . Finally, we also tested the impact of infection on the course of infection. Although strongly increases the frequency of IFNγ CD4 T cells, it does not ameliorate the control of infection, suggesting that it is not controlled by the same effector mechanisms as . Thus, whereas infections are commonly viewed as immunosuppressive and pathogenic, our data suggest that these parasites can specifically affect the immune control of infection, with benefits for the host.