Machelart Arnaud, Van Vyve Margaux, Potemberg Georges, Demars Aurore, De Trez Carl, Tima Hermann Giresse, Vanwalleghem Gilles, Romano Marta, Truyens Carine, Letesson Jean-Jacques, Muraille Eric
Unité de Recherche en Biologie des Microorganismes, Laboratoire d'Immunologie et de Microbiologie, NARILIS, Université de Namur, Namur, Belgium.
Department of Molecular and Cellular Interactions, Vlaams Interuniversitair Instituut voor Biotechnologie, Vrije Universiteit Brussel, Brussels, Belgium.
Front Immunol. 2017 Jul 31;8:903. doi: 10.3389/fimmu.2017.00903. eCollection 2017.
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 IFNγCD4 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.
本研究在小鼠中建立了一种原创的共感染模型，使用人类布鲁氏菌病最常见的病原体 ，以及非洲锥虫病的病原体 。尽管 在天然宿主和小鼠模型中的免疫抑制作用已得到充分证实，但我们观察到，向长期感染 的小鼠注射 会导致脾脏（感染的主要储存部位）中 的数量急剧减少。在感染 和 的小鼠以及感染 并同时感染 的小鼠中也获得了类似结果，表明这种现象并非由于抗原交叉反应。对共感染的野生型小鼠和基因缺陷小鼠的比较表明，清除 需要功能性的IL-12p35/IFNγ信号通路以及CD4 T细胞的存在。然而，野生型 和 的减毒突变体对 的影响相似，这表明清除 不需要慢性强烈的炎症反应。最后，我们还测试了 感染对 感染进程的影响。尽管 强烈增加了IFNγ CD4 T细胞的频率，但它并没有改善对 感染的控制，这表明它不受与 相同的效应机制控制。因此，尽管 感染通常被视为具有免疫抑制性和致病性，但我们的数据表明，这些寄生虫可以特异性地影响对 感染的免疫控制，对宿主有益。
