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首页> 外文期刊>Infection and immunity >Innate Immunity to the Pathogenic Fungus Coccidioides posadasii Is Dependent on Toll-Like Receptor 2 and Dectin-1
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Innate Immunity to the Pathogenic Fungus Coccidioides posadasii Is Dependent on Toll-Like Receptor 2 and Dectin-1

机译：病原性真菌球孢子虫的固有免疫力取决于Toll样受体2和Dectin-1。

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Coccidioides posadasii is a pathogenic fungus that causes endemic and epidemic coccidioidomycosis in the deserts of North, Central, and South America. How the innate immune system responds to the organism is not well understood. Here we show that elicited mouse peritoneal macrophages respond to spherules (the tissue form of the fungus) by producing proinflammatory cytokines as measured by quantitative PCR of cellular transcripts and by enzyme-linked immunosorbent assay (ELISA) assays for secreted protein. We examined the contribution of Toll-like receptors (TLR) and MyD88 in macrophage responses to formalin-killed spherules (FKS) by comparing cytokine responses of elicited macrophages from different knockout mice. FKS were added to elicited mouse peritoneal macrophages from wild-type, TLR2?/?, and MyD88?/? cells, and wild-type cells made more tumor necrosis factor alpha, MIP-2, and interleukin 6 than did the mutant macrophages. In contrast, the C3H/HeJ mice, which have a point mutation in TLR4, and TLR4?/? B6 mice exhibited no defect in cytokine production compared to the control mice. We also investigated the role of the macrophage β-glucan receptor, Dectin-1. RAW 264.7 macrophages overexpressing Dectin-1 produced more cytokines in respond to FKS, live spherules, and purified β-glucan than did control RAW cells. Blockage of Dectin-1 with antibodies inhibited cytokine production in elicited mouse peritoneal macrophages. Taken together, these results show that cytokine responses in mouse peritoneal macrophages to C. posadasii spherules are dependent on TLR2, MyD88, and Dectin-1.
机译： Coccidioides posadasii 是一种致病性真菌，在北美，中美洲和南美洲的沙漠中引起地方性和流行性球虫病。先天免疫系统如何对生物体产生反应尚不清楚。在这里，我们显示引起的小鼠腹膜巨噬细胞通过产生促炎性细胞因子来响应球体（真菌的组织形式），如通过细胞转录物的定量PCR和通过酶联免疫吸附测定（ELISA）测定分泌蛋白的方法来测量。我们通过比较不同敲除小鼠引起的巨噬细胞的细胞因子反应，研究了Toll样受体（TLR）和MyD88在巨噬细胞对福尔马林杀死的小球（FKS）反应中的作用。将FKS加入到野生型，TLR2 ？/？和MyD88 ？/？细胞引起的小鼠腹膜巨噬细胞中，野生型细胞产生更多的肿瘤坏死因子α ，MIP-2和白介素6比突变型巨噬细胞要大。相反，在TLR4中具有点突变的C3H / HeJ小鼠和TLR4 α/β B6小鼠与对照小鼠相比在细胞因子产生上没有缺陷。我们还研究了巨噬细胞β-葡聚糖受体Dectin-1的作用。与对照RAW细胞相比，过表达Dectin-1的RAW 264.7巨噬细胞对FKS，活球和纯化的β-葡聚糖产生更多的细胞因子。用抗体阻断Dectin-1可抑制小鼠腹腔巨噬细胞中细胞因子的产生。综上，这些结果表明，小鼠腹膜巨噬细胞中的细胞因子对 C的反应。 posadasii 小球依赖于TLR2，MyD88和Dectin-1。

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