IL-17 Is Necessary for Host Protection against Acute-Phase Trypanosoma cruzi Infection
IL-17 Is Necessary for Host Protection against Acute-Phase Trypanosoma cruzi Infection
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DOI：
10.4049/jimmunol.0900047
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发表时间：
2010-07-15
影响因子：
4.4
通讯作者：
Yoshida, Hiroki
中科院分区：
文献类型：
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作者：
Miyazaki, Yoshiyuki;Hamano, Shinjiro;Yoshida, Hiroki
IL-17 A是通过有组织地产生炎性细胞因子（如IL-6、TNF-α和GM-CSF）来诱导炎性应答并诱导嗜中性粒细胞迁移的关键细胞因子。IL-17 A在细胞内原生动物寄生虫感染中的作用尚未阐明，尽管IL-17 A增强的免疫应答对于解决一些细菌和真菌感染是重要的。因此，我们实验性地用克氏锥虫感染IL-17 A缺陷（IL-17 A（-/-））小鼠。与对照C57 BL/6野生型（WT）小鼠相比，IL-17 A（-/-）小鼠感染后存活率较低，寄生虫血症持续时间较长。与WT小鼠相比，在感染的IL-17 A（-/-）小鼠中观察到多器官衰竭，如组织损伤的血清学标志物（如天冬氨酸转氨酶）显著增加所反映的，这导致IL-17 A（-/-）小鼠死亡率增加。与WT小鼠相比，IL-17 A（-/-）小鼠的肝脏浸润细胞中细胞因子如IFN-γ、IL-6和TNF-α的表达较低。在中性粒细胞酶的表达中观察到类似的缺陷，如髓过氧化物酶和脂氧合酶，而细胞浸润到感染组织中不受IL-17 A缺乏的影响。这些结果表明，有效激活免疫相关细胞是T细胞杀伤的关键。cruzi在缺乏IL-17 A的情况下受损，导致这些小鼠对T.克氏感染从这些结果，我们得出结论，IL-17 A是重要的，为解决T。克氏感染免疫学杂志，2010，185：1150-1157。
IL-17A is a key cytokine that induces inflammatory responses through the organized production of inflammatory cytokines, such as IL-6, TNF-alpha, and GM-CSF, and induces neutrophil migration. The roles of IL-17A in infection of intracellular protozoan parasites have not been elucidated, although augmented immune responses by IL-17A are important for the resolution of some bacterial and fungal infections. Therefore, we experimentally infected IL-17A-deficient (IL-17A(-/-)) mice with Trypanosoma cruzi. IL-17A(-/-) mice had a lower survival rate and prolonged worse parasitemia compared with control C57BL/6 wild-type (WT) mice postinfection. In the infected IL-17A(-/-) mice, multiple organ failure was observed compared with WT mice, as reflected by the marked increase in serologic markers of tissue injury, such as aspartate aminotransferase, which resulted in increased mortality of IL-17A(-/-) mice. Expression of cytokines, such as IFN-gamma, IL-6, and TNF-alpha, was lower in liver-infiltrating cells from the IL-17A(-/-) mice compared with WT mice. A similar defect was observed in the expression of neutrophil enzymes, such as myeloperoxidase and lipoxygenase, whereas cellular infiltration into the infected tissues was not affected by IL-17A deficiency. These results suggested that the efficient activation of immune-related cells critical for the killing of T. cruzi was impaired in the absence of IL-17A, resulting in the greater susceptibility of those mice to T. cruzi infection. From these results, we conclude that IL-17A is important for the resolution of T. cruzi infection. The Journal of Immunology, 2010, 185: 1150-1157.