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首页> 外文期刊>Mediators of inflammation >The Role of Cytokines, Chemokines, and Growth Factors in the Pathogenesis of Pityriasis Rosea
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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玫瑰糠疹的发病机理中的作用

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Introduction. Pityriasis rosea (PR) is an exanthematous disease related to human herpesvirus- (HHV-) 6/7 reactivation. The network 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-)γ, tumor necrosis factor- (TNF-)α, 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-γ, 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-γhas 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。玫瑰糠疹(PR)是与人类疱疹病毒(HHV-)6/7激活有关的皮炎性疾病。尚未研究参与募集浸润性炎症细胞的介体网络。调查PR和健康对照组中血清细胞因子,生长因子和趋化因子的水平,以阐明PR的发病机理。材料和方法。白介素-(IL-)1,IL-6,IL-17,干扰素-(IFN-)γ,肿瘤坏死因子-(TNF-)α,血管内皮生长因子(VEGF),粒细胞集落刺激因子(G-CSF ),并通过多重测定在早期急性PR患者的血清和健康对照中同时测量趋化因子CXCL8(IL-8)和CXCL10(IP-10)。随后,在3个不同的时间(0、15和30天)对PR患者的血清进行了分析。结果与讨论。与对照组相比,PR患者的血清IL-17,IFN-γ,VEGF和IP-10水平升高。 IL-17在宿主防御病原体中起关键作用,病原体刺激促炎性细胞因子/趋化因子的释放。 IFN-γ具有直接的抗病毒活性,可促进NK细胞和病毒特异性T细胞的细胞毒性。 VEGF刺激血管生成和血管生成。 IP-10可以诱导趋化性,凋亡,细胞生长和血管生成。我们的发现表明,这些炎性介质可能以协同方式调节PR的发病机理。

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