...
首页> 外文期刊>Mediators of inflammation >The Role of Cytokines, Chemokines, and Growth Factors in the Pathogenesis of Pityriasis Rosea
【24h】

The Role of Cytokines, Chemokines, and Growth Factors in the Pathogenesis of Pityriasis Rosea

机译:细胞因子,趋化因子和生长因子在Pityriasis Rosea发病机制中的作用

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

Introduction. Pityriasis rosea (PR) is an exanthematous disease related to human herpesvirus-(HHV-) 6/7 reactivation. Thenetwork of mediators involved in recruiting the infiltrating inflammatory cells has never been studied. Object. To investigate the levels of serum cytokines, growth factors, and chemokines in PR and healthy controls in order to elucidate the PR pathogenesis. Materials and Methods. Interleukin-(IL-) 1, IL-6, IL-17, interferon-(IFN-)alpha, tumor necrosis factor-(TNF-)alpha, vascular endothelial growth factor (VEGF), granulocyte colony stimulating factor (G-CSF), and chemokines, CXCL8 (IL-8) and CXCL10 (IP-10), were measured simultaneously by a multiplex assay in early acute PR patients' sera and healthy controls. Subsequently, sera from PR patients were analysed at 3 different times (0, 15, and 30 days). Results and discussion. Serum levels of IL-17, IFN-gamma, VEGF, and IP-10 resulted to be upregulated in PR patients compared to controls. IL-17 has a key role in host defense against pathogens stimulating the release of proinflammatory cytokines/chemokines. IFN-gamma has a direct antiviral activity promoting NK cells and virus specific T cells cytotoxicity. VEGF stimulates vasculogenesis and angiogenesis. IP-10 can induce chemotaxis, apoptosis, cell growth, and angiogenesis. Conclusions. Our findings suggest that these inflammatory mediators may modulate PR pathogenesis in synergistic manner.
机译:介绍。 Pityriasis Rosea(PR)是与人疱疹病毒 - (HHV-)6/7重新激活有关的蛋白质疾病。从未研究过招募浸润炎症细胞的调解器的TheTwork。目的。为了阐明PR发病机制,探讨PR和健康对照中血清细胞因子,生长因子和趋化因子的水平。材料和方法。白细胞介素 - (IL-)1,IL-6,IL-17,干扰素 - (IFN-)α,肿瘤坏死因子 - (TNF-)α,血管内皮生长因子(VEGF),粒细胞菌落刺激因子(G-CSF )和趋化因子,CXCL8(IL-8)和CXC110(IP-10)通过早期急性PR患者血清和健康对照中的多重测定同时测量。随后,在3种不同的时间(0,15和30天)分析来自PR患者的血清。结果和讨论。与对照相比,在PR患者中导致血清IL-17,IFN-Gamma,VEGF和IP-10水平导致患者上调。 IL-17对刺激病原体的宿主防御具有关键作用,刺激释放促炎细胞因子/趋化因子。 IFN-Gamma具有促进NK细胞和病毒特异性T细胞细胞毒性的直接抗病毒活性。 VEGF刺激血管发生和血管生成。 IP-10可以诱导趋化性,细胞凋亡,细胞生长和血管生成。结论。我们的研究结果表明,这些炎症介质可以以协同方式调节PR发病机制。

著录项

  • 来源
    《Mediators of inflammation》 |2015年第6期|共6页
  • 作者单位

    IRCCS Azienda Osped Univ San Martino IST Sect Dermatol I-16132 Genoa Italy;

    IRCCS Azienda Osped Univ San Martino IST Sect Dermatol I-16132 Genoa Italy;

    Univ Milano Bicocca Fac Med &

    Surg Dept Hlth Sci Lab Microbiol &

    Virol I-20900 Monza Italy;

    IRCCS Azienda Osped Univ San Martino IST Dept Internal Med I-16132 Genoa Italy;

    IRCCS Azienda Osped Univ San Martino IST Dept Internal Med I-16132 Genoa Italy;

    IRCCS Azienda Osped Univ San Martino IST Sect Dermatol I-16132 Genoa Italy;

    IRCCS Azienda Osped Univ San Martino IST Sect Dermatol I-16132 Genoa Italy;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 病理学;
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号