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首页> 外文期刊>Infection and immunity >MyD88 Deficiency Leads to Decreased NK Cell Gamma Interferon Production and T Cell Recruitment during Chlamydia muridarum Genital Tract Infection, but a Predominant Th1 Response and Enhanced Monocytic Inflammation Are Associated with Infection Resolution
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MyD88 Deficiency Leads to Decreased NK Cell Gamma Interferon Production and T Cell Recruitment during Chlamydia muridarum Genital Tract Infection, but a Predominant Th1 Response and Enhanced Monocytic Inflammation Are Associated with Infection Resolution

机译：MyD88缺乏症导致muridarum衣原体生殖道感染期间NK细胞γ干扰素产生和T细胞募集减少，但主要的Th1反应和单核细胞炎症增强与感染的解决有关

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We have previously shown that MyD88 knockout (KO) mice exhibit delayed clearance of Chlamydia muridarum genital infection compared to wild-type (WT) mice. A blunted Th1 response and ineffective suppression of the Th2 response were also observed in MyD88 KO mice. The goal of the present study was to investigate specific mechanisms whereby absence of MyD88 leads to these effects and address the compensatory mechanisms in the genital tract that ultimately clear infection in the absence of MyD88. It was observed that NK cells recruited to the genital tract in MyD88 KO mice failed to produce gamma interferon (IFN-γ) mRNA and protein. This defect was associated with decreased local production of interleukin-17 (IL-17), IL-18, and tumor necrosis factor alpha (TNF-α) but normal levels of IL-12p70. Additionally, recruitment of CD4 T cells to the genital tract was reduced in MyD88 KO mice compared to that in WT mice. Although chronic infection in MyD88 KO mice resulted in oviduct pathology comparable to that of WT mice, increased histiocytic inflammation was observed in the uterine horns. This was associated with increased CCL2 levels and recruitment of macrophages as a potential compensatory mechanism. Further deletion of TLR4-TRIF signaling in MyD88 KO mice, using TLR4/MyD88 double-KO mice, did not further compromise host defense against chlamydiae, suggesting that compensatory mechanisms are Toll-like receptor (TLR) independent. Despite some polarization toward a Th2 response, a Th1 response remained predominant in the absence of MyD88, and it provided equivalent protection against a secondary infection as observed in WT mice.
机译：先前我们已经证明，与野生型（WT）小鼠相比，MyD88基因敲除（KO）小鼠展现出 muridarum 生殖器感染的清除延迟。在MyD88 KO小鼠中也观察到钝化的Th1反应和Th2反应的无效抑制。本研究的目的是研究不存在MyD88会导致这些效应的特定机制，并解决生殖道中的补偿机制，该机制最终会在不存在MyD88的情况下清除感染。观察到，在MyD88 KO小鼠中募集到生殖道的NK细胞未能产生γ干扰素（IFN-γ）mRNA和蛋白质。该缺陷与白细胞介素17（IL-17），IL-18和肿瘤坏死因子α（TNF-α）的局部产生减少有关，但IL-12p70水平正常。另外，与WT小鼠相比，MyD88 KO小鼠中CD4 T细胞向生殖道的募集减少。尽管MyD88 KO小鼠的慢性感染导致输卵管病理学与WT小鼠相当，但在子宫角中观察到组织细胞炎症增加。这与增加的CCL2水平和募集巨噬细胞作为潜在的补偿机制有关。使用TLR4 / MyD88 double-KO小鼠在MyD88 KO小鼠中进一步删除TLR4-TRIF信号转导不会进一步损害宿主对衣原体的防御，这表明补偿机制是独立于Toll样受体（TLR）的。尽管对Th2应答存在两极分化，但在不存在MyD88的情况下，Th1应答仍然占主导地位，与WT小鼠中观察到的一样，Th1应答提供了对继发感染的等同保护。

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