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Trypanosoma infection favors Brucella elimination via IL-12/IFNγ-dependent pathways

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DOI

  • Arnaud Machelart, Universite de Namur
  • ,
  • Margaux Van Vyve, Universite de Namur
  • ,
  • Georges Potemberg, Universite de Namur
  • ,
  • Aurore Demars, Universite de Namur
  • ,
  • Carl De Trez, Flanders Institute for Biotechnology
  • ,
  • Hermann Giresse Tima, Scientific Institute of Public Health, Brussels
  • ,
  • Gilles Vanwalleghem
  • Marta Romano, Scientific Institute of Public Health, Brussels
  • ,
  • Carine Truyens, Université Libre de Bruxelles
  • ,
  • Jean Jacques Letesson, Universite de Namur
  • ,
  • Eric Muraille, Universite de Namur, Université Libre de Bruxelles

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

Original languageEnglish
Article number903
JournalFrontiers in Immunology
Volume8
IssueJUL
ISSN1664-3224
DOIs
Publication statusPublished - 31 Jul 2017
Externally publishedYes

Bibliographical note

Funding Information:
The authors thank Fabienne Jurion (WIV-ISP) for her expert technical assistance and Aurore Lison and Alain Wathelet-Depauw for their helpful contribution. This work was supported by grants from the Fonds National de la Recherche Scientifique (FNRS) (convention FRSM FNRS 3.4.600.06.F, Belgium) and by the Interuniversity Attraction Poles Programme initiated by the Belgian Science Policy Office. EM is a Senior Research Associate from the FRS-FNRS (Belgium). AM holds FRIA PhD grants from the FRS-FNRS (Belgium).

Publisher Copyright:
© 2017 Machelart, Van Vyve, Potemberg, Demars, De Trez, Tima, Vanwalleghem, Romano, Truyens, Letesson and Muraille.

    Research areas

  • Brucella abortus, Brucella melitensis, Brucellosis, Infection control, Mycobacterium tuberculosis, Trypanosoma brucei brucei, Trypanosoma cruzi

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