首页> 外文期刊>European cytokine network >Sustained parasite burden in the spleen of Leishmania infantum-infected BALB/c mice is accompanied by expression of MCP-1 transcripts and lack of protection against challenge.
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Sustained parasite burden in the spleen of Leishmania infantum-infected BALB/c mice is accompanied by expression of MCP-1 transcripts and lack of protection against challenge.

机译:婴儿利什曼原虫感染的BALB / c小鼠脾脏中持续存在的寄生虫负担伴随着MCP-1转录本的表达和对攻击的缺乏保护。

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摘要

We analyzed differential responses of spleen and liver, major organ targets for viscerotropic Leishmania species, to experimental infection and examined if resistance to challenge was organ-specific. In liver, parasites were spontaneously cleared and iNOS trancripts expression paralleled that of amastigote load. In the spleen, amastigote multiplication was only partly controlled, and iNOS transcripts expression was transient. Total numbers of spleen cells, B cells, and T cells were decreased, while F4/80(+) and Mac1(+) cells were conserved. Expression of splenic MCP-1 transcripts remained constant, indicating its possible contribution to immigration of Leishmania host cells and to sustained parasite load. Spleen cells produced both, Th1- and Th2-type cytokines and Th2-type response was dominant, compatible with the sustained MCP-1 expression. Challenge experiments showed that in contrast to the liver, where initial infection conferred a progressively established immunity, in the spleen there was no induced protection against reinfection. Organ-specific resistance against challenge could be important for designing antileishmanial vaccines.
机译:我们分析了脾脏和肝脏(内脏利什曼原虫物种的主要器官靶标)对实验感染的不同反应,并检查了对攻击的抵抗性是否是器官特异性的。在肝脏中,寄生虫被自发清除,iNOS转录物表达与假肢孢子虫负荷相似。在脾脏中,鞭毛体的增殖仅受到部分控制,iNOS转录物的表达是短暂的。脾细胞,B细胞和T细胞总数减少,而F4 / 80(+)和Mac1(+)细胞得以保存。脾脏MCP-1转录物的表达保持恒定,表明其可能对利什曼原虫宿主细胞的迁移和持续的寄生虫负荷做出了贡献。脾细胞产生Th1型和Th2型细胞因子,并且Th2型应答占主导,与持续的MCP-1表达相容。挑战实验表明,与肝脏不同,在肝脏中最初的感染赋予了逐渐建立的免疫力,而在脾脏中则没有诱导的针对再感染的保护作用。器官对攻击的抗性对于设计抗疟疾疫苗可能很重要。

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