Hepatitis C virus and alcoholic liver disease are major causes of chronic liver diseases worldwide. Little is known about differences between chronic hepatitis C and alcoholic liver disease in terms of lymphocytes' sub-population. Aim of the present study was to compare the sub-populations of lymphocytes in both ascitic compartment and peripheral blood in patients with decompensated liver cirrhosis due to chronic hepatitis C and alcoholic liver disease. Patients with decompensated liver cirrhosis due to hepatitis C virus or alcoholic liver disease evaluated from April 2014 to October 2016 were enrolled. Whole blood and ascitic fluid samples were stained with monoclonal antibodies specific for human TCRɑβ, TCRɣδ, CD3, CD4, CD8, CD19, CCR6, CD16, CD56, CD25, HLA-DR, Vɑ24. Sixteen patients with decompensated liver cirrhosis were recruited (9 with hepatitis C virus and 7 with alcoholic liver disease). In ascitic fluid, the percentage of both CD3+CD56- and CD3+CD56+iNKT cells resulted higher in hepatitis C virus patients than in alcoholic liver disease patients (1.82 ± 0.35% vs 0.70 ± 0.42% (p < 0.001) and 1.42 ± 0.35% vs 0.50 ± 0.30% (p < 0.001), respectively). Conversely, in peripheral blood samples, both CD3+CD56- and CD3+CD56+iNKT cells resulted significantly higher in alcoholic liver disease than in hepatitis C virus patients (4.70 ± 2.69% vs 1.50 ± 1.21% (p < 0.01) and 3.10 ± 1.76% vs 1.00 ± 0.70% (p < 0.01), respectively). Both elevation of iNKT cells in ascitic fluid and reduction in peripheral blood registered in hepatitis C virus but not in alcoholic liver disease patients might be considered indirect signals of tissutal translocation. In conclusion, we described relevant differences between the two groups. Alcoholic liver disease patients displayed lower number of CD3+CD4+ cells and a higher percentage of CD3-CD16+, Vα24+CD3+CD56- and Vα24+CD3+CD56+iNKT cells in ascitic fluid than hepatitis C virus positive subjects. Further studies might analyze the role of immune cells in the vulnerability toward infections and detect potential targets for new treatments especially for alcoholic liver disease patients.

译文

丙型肝炎病毒和酒精性肝病是全球慢性肝病的主要原因。对于慢性丙型肝炎和酒精性肝病之间在淋巴细胞亚群方面的差异知之甚少。本研究的目的是比较因慢性丙型肝炎和酒精性肝病而失代偿期肝硬化患者腹水室和外周血中淋巴细胞的亚群。从2014年4月到2016年10月评估的因丙型肝炎病毒或酒精性肝病而失代偿性肝硬化患者被纳入。全血和腹水样品用对人tcr ɑ β,tcr ɑ δ,CD3,CD4,CD8,CD19,CCR6,CD16,CD56,CD25,hla-dr,v ɑ 24具有特异性的单克隆抗体染色。招募了16例失代偿期肝硬化患者 (9例患有丙型肝炎病毒,7例患有酒精性肝病)。在腹水中,丙型肝炎病毒患者CD3 + CD56-和CD3 + CD56 + iNKT细胞的百分比高于酒精性肝病患者 (1.82   ±   0.35% vs 0.70   ±   0.42% (p  <  0.001) 和1.42   ±   0.35% vs 0.50   ±   0.30% (p  <  0.001),分别)。相反,在外周血样本中,酒精性肝病患者的CD3 CD56-和CD3 CD56 iNKT细胞均显着高于丙型肝炎病毒患者 (4.70   ±   2.69% vs 1.50   ±   1.21% (p  <  0.01) 和3.10   ±   1.76% vs 1.00   ±   0.70% (p  <  0.01),分别)。腹水中iNKT细胞的升高和丙型肝炎病毒 (但酒精性肝病患者未注册) 的外周血减少都可能被认为是组织易位的间接信号。总之,我们描述了两组之间的相关差异。与丙型肝炎病毒阳性受试者相比,酒精性肝病患者腹水中CD3 CD4细胞的数量较低,CD3-CD16,Vα24 CD3 CD56-和Vα24 CD3 CD56 iNKT细胞的百分比较高。进一步的研究可能会分析免疫细胞在感染易感性中的作用,并发现新疗法的潜在靶标,尤其是对于酒精性肝病患者。

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