Early infection with Leishmania major restrains pathogenic response to Leishmania amazonensis and parasite growth
Early infection with Leishmania major restrains pathogenic response to Leishmania amazonensis and parasite growth
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DOI：
10.1016/j.actatropica.2007.12.012
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发表时间：
2008-04-01
期刊：
影响因子：
2.7
通讯作者：
Vieira, L. Q.
中科院分区：
文献类型：
--
作者：
Gonzalez-Lombana, C. Z.;Santiago, H. C.;Vieira, L. Q.
利什曼原虫感染的实验模型为宿主抑制寄生虫生长的耐药机制中涉及的几个免疫事件提供了知识。人们普遍认为存在伴随免疫，并且有一些证据表明它将在长期获得性感染抗性中发挥重要作用。本文研究了大利什曼原虫感染C57BL/6小鼠对亚马逊利什曼原虫感染的抗性。C57BL/6小鼠在感染L major之前和之后的不同时间感染亚马孙乳杆菌，该小鼠自愈。结果表明，C57BL/6小鼠感染了L. major后，可抑制L. amazonensis感染引起的致病反应，并将寄生虫负荷降低一个数量级。联合感染小鼠的病变中ifn - γ的产生与单独感染L. major的小鼠相似，但观察到更高的tnf - α和一氧化氮合酶（NOS） mRNA表达。令人惊讶的是，受抑制的致病反应与IL-10的产生无关，这一点可以从共同感染小鼠的病变和IL-10（-/-）共同感染小鼠的mRNA和蛋白表达水平降低中得到证明。感染部位的炎症浸润检查显示亚马逊河蛭病变中单核细胞和淋巴细胞数量减少。此外，还观察到CCL3/MIP-1 α和CCL5/RANTES的差异产生。我们认为亚马孙乳杆菌对C57BL/6小鼠预感染亚马孙乳杆菌后病变进展的控制与在亚马孙乳杆菌感染部位诱导下调环境有关。(C) 2008 Elsevier B.V.版权所有
Experimental models of infection with Leishmania spp. have provided knowledge of several immunological events involved in the resistance mechanism used by the host to restrain parasite growth. It is well accepted that concomitant immunity exists, and there is some evidence that it would play a major role in long-lasting acquired resistance to infection. In this paper, the resistance to Leishmania amazonensis infection in C57BL/6 mice infected with Leishmania major was investigated. C57BL/6 mice, which spontaneously heal lesions caused by infection with L major, were infected with L. amazonensis at different times before and after L. major. We demonstrated that C57BL/6 mice previously infected with L. major restrain pathogenic responses induced by L. amazonensis infection and decrease parasite burdens by one order of magnitude. Co-infected mice showed production of IFN-gamma in lesions similar to mice infected solely with L. major, but higher TNF-alpha and nitric oxide synthase (NOS) mRNA expression was observed. Surprisingly, the restrained pathogenic response was not related to IL-10 production, as evidenced by lower levels of both mRNA, protein expression in lesions from co-infected mice and in co-infections in IL-10(-/-) mice. Examination of the inflammatory infiltrate at the site of infection showed a reduced number of monocytes and lymphocytes in L. amazonensis lesions. Additionally, differential production of the CCL3/MIP-1 alpha and CCL5/RANTES was observed. We suggest that the control of lesion progression caused by L. amazonensis in C57BL/6 mice pre-infected with L. major is related to the induction of a down-regulatory environment at the site of infection with L. amazonensis. (C) 2008 Elsevier B.V. All rights reserved.