Chlamydial Lipoproteins Stimulate Toll-Like Receptors 1/2 Mediated Inflammatory Responses through MyD88-Dependent Pathway.
Chlamydial Lipoproteins Stimulate Toll-Like Receptors 1/2 Mediated Inflammatory Responses through MyD88-Dependent Pathway.
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衣原体脂蛋白通过 MyD88 依赖性途径刺激 Toll 样受体 1/2 介导的炎症反应
DOI：
10.3389/fmicb.2017.00078
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发表时间：
2017
影响因子：
5.2
通讯作者：
Wu X
中科院分区：
文献类型：
--
作者：
Wang Y;Liu Q;Chen D;Guan J;Ma L;Zhong G;Shu H;Wu X
衣原体是一种非常重要的病原体，可引起人类多种疾病，但其致病机制尚不清楚。为了阐明衣原体脂蛋白诱导的宿主炎症反应和信号通路，测试了预测的沙眼衣原体脂蛋白诱导小鼠巨噬细胞或人TLR（Toll样受体）表达细胞系释放促炎细胞因子的能力。结果表明，重组C.沙眼衣原体D381、D541、D 067和D 775在TLR表达细胞系中显示出强烈的诱导IL-8释放的能力。信号通路涉及TLR 1/2和TLR 2/CD 14，但不涉及TLR 4。此外，除D 067外，D381、D541和D 775的促炎细胞因子诱导需要硫代酰化位点（半胱氨酸）进行脂质修饰，并且诱导是通过MyD 88介导的途径。提示脂蛋白在C.沙眼通过TLR途径诱导的炎症反应。这是第一个研究，以其他衣原体脂蛋白后，确定的作用，MIP（D541）的衣原体疾病的发病机制。
Chlamydiae are very important pathogens which could cause several types of diseases in human, but little is known about its pathogenic mechanism. In order to elucidate host inflammatory response and the signal pathway induced by Chlamydial lipoproteins, the predicted lipoproteins of Chlamydia trachomatis were tested for their ability to induce the release of proinflammatory cytokines by mouse macrophages or human TLR (Toll-Like Receptor) expressing cell lines. The results showed that recombinant proteins of C. trachomatis D381, D541, D067, and D775 displayed a strong ability to induce the release of IL-8 in TLR expressing cell line. The signal pathways involved TLR1/2 and TLR2/CD14 but not TLR4. Moreover, except D067, the proinflammatory cytokine induction by D381, D541, and D775 required the thioacylation site (cysteine) for lipid modification and the induction was through MyD88-mediated pathway. Our data supported that lipoproteins played a vital role in pathogenesis of C. trachomatis-induced inflammatory responses via TLR pathway. It was the first study to characterize other chlamydial lipoproteins after identifying the role of MIP (D541) on pathogenesis of Chlamydial diseases.