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首页> 外文期刊>Infection and immunity >Interleukin-23 (IL-23)-IL-17 Cytokine Axis in Murine Pneumocystis carinii Infection
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Interleukin-23 (IL-23)-IL-17 Cytokine Axis in Murine Pneumocystis carinii Infection

机译：鼠卡氏肺囊虫感染中的白介素23（IL-23）-IL-17细胞因子轴

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Host defense mechanisms against Pneumocystis carinii are not fully understood. Previous work in the murine model has shown that host defense against infection is critically dependent upon host CD4+ T cells. The recently described Th17 immune response is predominantly a function of effector CD4+ T cells stimulated by interleukin-23 (IL-23), but whether these cells are required for defense against P. carinii infection is unknown. We tested the hypothesis that P. carinii stimulates the early release of IL-23, leading to increases in IL-17 production and lung effector CD4+ T-cell population that mediate clearance of infection. In vitro, stimulation of alveolar macrophages with P. carinii induced IL-23, and IL-23p19 mRNA was expressed in lungs of mice infected with this pathogen. To address the role of IL-23 in resistance to P. carinii, IL-23p19?/? and wild-type control C57BL/6 mice were infected and their fungal burdens and cytokine/chemokine responses were compared. IL-23p19?/? mice displayed transient but impaired clearance of infection, which was most apparent 2 weeks after inoculation. In confirmatory studies, the administration of either anti-IL-23p19 or anti-IL-17 neutralizing antibody to wild-type mice infected with P. carinii also caused increases in fungal burdens. IL-17 and the lymphocyte chemokines IP-10, MIG, MIP-1α, MIP-1β, and RANTES were decreased in the lungs of infected IL-23p19?/? mice in comparison to their levels in the lungs of wild-type mice. In IL-23p19?/? mice infected with P. carinii, there were fewer effector CD4+ T cells in the lung tissue. Collectively, these studies indicate that the IL-23-IL-17 axis participates in host defense against P. carinii.
机译：尚未完全了解针对卡氏肺孢子虫的宿主防御机制。鼠模型的先前工作表明，宿主对感染的防御至关重要地依赖于宿主CD4 + T细胞。最近描述的Th17免疫应答主要是由白介素23（IL-23）刺激的效应CD4 + T细胞的功能，但这些细胞是否是防御 P所必需的。 carinii 感染未知。我们检验了 P的假设。卡里尼氏菌刺激IL-23的早期释放，导致IL-17产生增加以及介导感染清除的肺效应CD4 + T细胞群体。在体外，用 P刺激肺泡巨噬细胞。卡林氏菌诱导的IL-23和IL-23p19 mRNA在感染该病原体的小鼠肺中表达。解决IL-23在抗 P中的作用。 carinii ，IL-23p19？/？感染了野生型和对照C57BL / 6的小鼠，比较了它们的真菌负担和细胞因子/趋化因子的反应。 IL-23p19？/？小鼠表现出短暂的但清除感染的能力受损，这在接种后2周最为明显。在验证性研究中，将抗IL-23p19或抗IL-17中和抗体给予感染了 P的野生型小鼠。卡里氏菌也引起真菌负担增加。在感染的IL-23p19α/β肺中，IL-17和淋巴细胞趋化因子IP-10，MIG，MIP-1α，MIP-1β和RANTES降低。与它们在野生型小鼠肺中的水平相比。在IL-23p19中？感染 P的小鼠。 Carinii ，肺组织中的效应CD4 + T细胞较少。总的来说，这些研究表明IL-23-IL-17轴参与了针对 P的宿主防御。卡林氏。

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