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首页> 外文期刊>Internal and Emergency Medicine >Elevated serum levels of decoy receptor 3 are associated with disease severity in patients with hemorrhagic fever with renal syndrome
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Elevated serum levels of decoy receptor 3 are associated with disease severity in patients with hemorrhagic fever with renal syndrome

机译:肾综合征出血热患者血清中诱饵受体3的升高与疾病的严重程度相关

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摘要

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral infectious disease characterized by fever, hemorrhage and renal failure. HFRS has become a serious public health problem in China. Unfortunately, the pathogenesis of HFRS has not been completely clarified. The aim of this study is to investigate the changes of decoy receptor 3 (DcR3) and to further explore its potential roles in HFRS. The levels of serum DcR3 were measured by sandwich ELISA. We found serum DcR3 levels increased significantly, which reached peak value during the oliguric phase and in the critical group. Moreover, serum DcR3 levels were closely related to the levels of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and parameters reflecting kidney injury including BUN, creatinine (Cr) and proteinuria. This study indicates that high levels of serum DcR3 have associations with the disease stages, severity and degree of kidney damage. Meanwhile, our results suggest that DcR3 may play a dual role in HFRS pathogenesis. First, DcR3 is involved in the inflammatory cascade response resulting in capillary permeability and kidney injury in the early stage. Secondly, HTNV infection induced DcR3 expression at the convalescent phase may act as a feed-back mechanism in anti-inflammatory response. Thus, a study of DcR3 is essential for a better understanding of HFRS pathogenesis.
机译:肾综合征出血热(HFRS)是一种以发烧,出血和肾衰竭为特征的急性病毒感染性疾病。 HFRS已成为中国严重的公共卫生问题。不幸的是,HFRS的发病机理尚未完全阐明。这项研究的目的是调查诱饵受体3(DcR3)的变化,并进一步探讨其在HFRS中的潜在作用。通过夹心ELISA测量血清DcR3的水平。我们发现血清DcR3水平显着升高,在少尿期和临界组达到峰值。此外,血清DcR3水平与促炎细胞因子肿瘤坏死因子-α(TNF-α)的水平以及反映肾脏损伤的参数(包括BUN,肌酐(Cr)和蛋白尿)密切相关。这项研究表明,高水平的血清DcR3与疾病阶段,严重程度和肾脏损害程度有关。同时,我们的结果表明DcR3可能在HFRS发病机理中起双重作用。首先,DcR3参与炎症级联反应,从而在早期导致毛细血管通透性和肾脏损伤。其次,HTNV感染在恢复期诱导的DcR3表达可能是抗炎反应的一种反馈机制。因此,对DcR3的研究对于更好地了解HFRS发病机理至关重要。

著录项

  • 来源
    《Internal and Emergency Medicine 》 |2015年第5期| 567-573| 共7页
  • 作者单位

    Department of Immunology and Pathogenic Biology School of Medicine Xi’an Jiaotong University">(1);

    Department of Immunology and Pathogenic Biology School of Medicine Xi’an Jiaotong University">(1);

    Department of Immunology and Pathogenic Biology School of Medicine Xi’an Jiaotong University">(1);

    Department of Ophthalmology Xi’an No. 4 Hospital">(2);

    Clinical Laboratory The Second Affiliated Hospital of Xi’an Jiaotong University">(3);

    Department of Immunology and Pathogenic Biology School of Medicine Xi’an Jiaotong University">(1);

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    DcR3; HFRS; TNF-α; HTNV;

    机译:DcR3;HFRS;TNF-α;越南国家电视台;

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