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Increases in intrahepatic CD68 positive cells, MAC387 positive cells, and proinflammatory cytokines (particularly interleukin 18) in chronic hepatitis C infection

机译：慢性丙型肝炎感染时肝内CD68阳性细胞，MAC387阳性细胞和促炎细胞因子（尤其是白介素18）的增加

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BACKGROUND—Upregulation of Th1 associated intrahepatic cytokines in chronic hepatitis C virus (HCV) infection should lead to a significant non-specific cellular immune response, a prerequisite for viral clearance. However, to date, the role of this non-specific response in HCV has been understudied.
AIMS—To analyse the intrahepatic macrophage activity in chronic HCV infection by immunostaining and by quantitation of cytokine mRNA.
METHODS—HCV positive liver tissues (chronic hepatitis, n=10; cirrhosis, n=5) were immunostained for CD68, MAC387, and semiquantitated by polymerase chain reaction for intrahepatic cytokine mRNAs (interferon γ (IFNγ), interleukin 1β (IL-1β), IL-6, IL-18, tumour necrosis factor α (TNFα), and macrophage inflammatory protein 1β (MIP1β)). HCV negative normal liver tissues (for cytokines, n=6; for immunostaining, n=5) were included as controls.
RESULTS—MAC387+ cells were focally increased in areas of erosion at the limiting plate while lobular staining was minimal. CD68+ staining was diffuse in both portal (increased in HCV) and lobular areas. The portal tract (mean) density of CD68+ and MAC387+ cells was significantly increased in patients with HCV compared with normal tissue. IFNγ and IL-18 mRNA levels were highly correlated and significantly upregulated in chronic hepatitis and cirrhotic tissue versus controls. TNFα mRNA was upregulated in chronic hepatitis without cirrhosis, while IL-6 mRNA was significantly downregulated. IL-1β, IL-6, and MIP1β mRNA levels were significantly correlated with portal tract MAC387+ cell density.
CONCLUSIONS—The significant upregulation of IFNγ and IL-18 mRNA and significant correlations between IFNγ and other proinflammatory cytokines, suggest a Th1/cell mediated intrahepatic immune response in chronic HCV infection. However, further clarification of the cellular sources of these cytokines is required.


Keywords: hepatitis C; macrophage; cytokine; interleukin; MAC387
机译：背景—慢性丙型肝炎病毒（HCV）感染中Th1相关肝内细胞因子的上调应导致明显的非特异性细胞免疫应答，这是病毒清除的前提。但是，迄今为止，这种非特异性应答在HCV中的作用尚未得到充分研究。目的：通过免疫染色和定量细胞因子mRNA分析慢性HCV感染中肝内巨噬细胞的活性。方法—对HCV阳性肝组织（慢性肝炎，n = 10；肝硬化，n = 5）进行CD68，MAC387免疫染色，并通过聚合酶链反应半定量检测肝内细胞因子mRNA（干扰素γ（IFNγ），白介素1β（IL-1β） ），IL-6，IL-18，肿瘤坏死因子α（TNFα）和巨噬细胞炎性蛋白1β（MIP1β））。 HCV阴性正常肝组织（对于细胞因子，n = 6；对于免疫染色，n = 5）作为对照。结果：在限制板的侵蚀区域，MAC387 +细胞局部增加，而小叶染色最小。 CD68 +染色弥漫在门静脉（HCV增加）和小叶区域。与正常组织相比，HCV患者的CD68 +和MAC387 +细胞的门静脉（平均）密度显着增加。与对照组相比，慢性肝炎和肝硬化组织中的IFNγ和IL-18 mRNA水平高度相关且显着上调。在没有肝硬化的慢性肝炎中，TNFαmRNA上调，而IL-6 mRNA显着下调。 IL-1β，IL-6和MIP1βmRNA水平与门道MAC387 +细胞密度显着相关。结论—IFNγ和IL-18 mRNA的显着上调以及IFNγ与其他促炎细胞因子之间的显着相关性表明在慢性HCV感染中Th1 /细胞介导的肝内免疫应答。但是，需要进一步澄清这些细胞因子的细胞来源。关键词：丙型肝炎；巨噬细胞细胞因子白介素MAC387

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