首页> 外文期刊>Journal of viral hepatitis. >Hepatic inflammatory cytokine mRNA expression in hepatitis C virus-human immunodeficiency virus co-infection.
【24h】

Hepatic inflammatory cytokine mRNA expression in hepatitis C virus-human immunodeficiency virus co-infection.

机译:丙型肝炎病毒-人免疫缺陷病毒共感染中肝炎性细胞因子mRNA的表达。

获取原文
获取原文并翻译 | 示例
       

摘要

Although epidemiologic studies have documented that hepatitis C virus (HCV)/human immunodeficiency virus (HIV) co-infected patients have accelerated fibrogenesis, especially those with CD4+ cell counts <200 cells/mm(3), the pathogenic mechanisms are poorly understood. We investigated whether severe immunodeficiency in co-infection is associated with changes in intrahepatic inflammatory cytokine mRNA levels. We measured interferon (IFN)-gamma, tumour necrosis factor-alpha, transforming growth factor (TGF)-beta(1), interleukin (IL)-4, IL-10, IL-12p35 and IL-12p40 mRNA levels by real-time PCR performed on liver samples from HCV mono-infected (n = 19) and HCV/HIV co-infected (n = 24) patients. Co-infected patients had decreased intrahepatic mRNA levels of IFN-gamma (P = 0.09), IL-4 (P 0.05) and IL-12p35 (P was increased (P = 0.07). In co-infected patients, IFN-gamma mRNA levels increased linearly with increasing peripheral CD4+ cell counts by 1.23 times relative to the calibrator for every 100 CD4+ cells/mm(3) increase (P = 0.02). No other cytokines were significantly associated with CD4+ cell counts. In conclusion, HIV-induced lymphopenia may result in hepatic inflammatory cytokine suppression in HCV/HIV co-infection. Intrahepatic IFN-gamma levels are significantly reduced in patients with advanced immunodeficiency. Further studies are needed to assess whether decreased IFN-gamma secretion by HCV-specific CD4+ cells may account for accelerated fibrogenesis in these patients.
机译:尽管流行病学研究表明,丙型肝炎病毒(HCV)/人免疫缺陷病毒(HIV)合并感染的患者加速了纤维生成,尤其是那些CD4 +细胞计数<200细胞/ mm的患者(3),但其致病机理却鲜为人知。我们调查了共感染中严重的免疫缺陷是否与肝内炎性细胞因子mRNA水平的变化有关。我们通过真实的方法测量了干扰素(IFN)-γ,肿瘤坏死因子-α,转化生长因子(TGF)-β(1),白介素(IL)-4,IL-10,IL-12p35和IL-12p40 mRNA的水平,在分别感染HCV单次感染(n = 19)和HCV / HIV共同感染(n = 24)的患者的肝脏样品上进行PCR检测的时间。在合并感染的患者中,IFN-γ的肝内mRNA水平降低(P = 0.09),IL-4(P = 0.05)和IL-12p35(P升高(P = 0.07))。相对于校准物,每增加100个CD4 +细胞/ mm(3),其水平就会线性增加,相对于校准品而言,增加了1.23倍(P = 0.02),没有其他细胞因子与CD4 +细胞数量显着相关。淋巴细胞减少症可能导致HCV / HIV合并感染中的肝炎性细胞因子抑制。晚期免疫缺陷患者肝内IFN-γ水平显着降低。还需要进一步研究以评估HCV特异性CD4 +细胞分泌的IFN-γ减少是否可能在这些患者中促进纤维发生。

著录项

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