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Toll3受体在呼吸道合胞病毒感染中作用的实验研究(1)
http://www.100md.com 2012年2月5日 杨宝顺 丁佳峰
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     [摘要] 目的 探讨呼吸道合胞病毒(RSV)感染人肺上皮A549细胞后,Toll样受体3(TLR3)的水平变化及其产生的Ⅰ型干扰素的抗病毒作用。 方法 RSV感染体外培养的人肺上皮A549细胞,并给予TLR3特异性抗体处理,分别感染4 h、8 h、12 h、16 h和24 h后收集各组细胞。未感染病毒的细胞作为对照组。RT-PCR法检测TLR3、IFN-α、IFN-β,RSV F蛋白的mRNA表达水平变化。 结果 RSV感染A549细胞后,TLR3、IFN-α、IFN-β,RSV F蛋白的mRNA表达量均升高且有时间依赖性。 结论 RSV感染A549细胞后可上调TLR3表达,其活化细胞介导产生的Ⅰ型干扰素能起到抗病毒作用。

    [关键词] 呼吸道合胞病毒;Toll样受体3;Ⅰ型干扰素

    [中图分类号] R562 [文献标识码] A [文章编号] 1673-9701(2012)04-0004-02

    Toll-like receptor 3 in the respiratory syncytial virus infection of the experimental study

    YANG Baoshun DING Jiafeng

    Department of Pediatrics, the First People's Hospital of Wenling City, Zhejiang Province, Wenling 317500, China

    [Abstract] Objective To understand the production mechanism of interferon and provide a scientific basis for prevention and clinical therapy. The expression changes of Toll-like receptor (TLR3) mRNA and the role of TLR3 in human lung epithelial cells (A549 cells) infected with respiratory syncytial virus (RSV) were investigated in this study. Methods RSV infected A549 cells were treated with or without specific antibodies of TLR3 and collected at the selected timepoints after RSV infection (4 h, 8 h, 12 h, 16 h and 24 h). The expressions of TLR3, IFN-α, IFN-β and RSV F mRNA were evaluated by RT-PCR. Results It was found that RSV infection could markedly up-regulate the mRNA expression of TLR3. Conclusion Above data indicate that RSV infection could induce an apparent increase of antiviral genes of IFN-α and IFN-β by activating TLR3 in human lung epithelial cells and the activated cells mediated Type I interferon is antiviral, which suggesting that TLR3 might play an important role in antiviralactivity of RSV-infected human lung epithelial cells.

    [Key words] Respiratory syncytial virus; Toll-like receptor 3; Type I interferon

    呼吸道合胞病毒(respiratory syncytial virus,RSV)在引起儿童尤其婴幼儿急性下呼吸道感染的病原中占主导地位,大约80%的毛细支气管炎和50%的婴幼儿肺炎由RSV所致。RSV感染后患儿临床症状较重,可导致呼吸衰竭和心力衰竭等并发症[1]。另外,RSV感染数月后易出现反复喘息症状,甚至发展成为婴幼儿哮喘。其发病机制可能与RSV感染造成呼吸道上皮细胞损伤、免疫功能紊乱、气道的神经调节失调有关[2]。目前对RSV感染尚无特殊有效的治疗和预防方案,抗炎与抗病毒仍为目前首选的治疗方法[3]。RSV为副粘病毒科肺炎病毒属,Toll样受体3(Toll-like receptor 3,TLR3)能特异性地识别双链RNA ......

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