Abstract
IntroductionLiver fibrosis is a result of continuous damage to the liver combined with accumulation of the extracellular matrix and is characteristic of most chronic liver diseases such as hepatitis C virus (HCV) infection.MethodsThis study evaluated interleukin 10 (IL10) expression in the liver and plasma of 45 HCV patients and its association with the pathogenesis and progression of liver fibrosis. The expression of transforming growth factor beta (TGFB1) was also assessed. Patients were divided into three groups according to the METAVIR classification (F0-F1, F2 and F3-F4); there was also a control group (n = 8).ResultsIn the control group, high intrahepatic IL10 mRNA expression showed a positive association with F0-F1 fibrosis, no inflammation, low concentrations of liver enzymes and a high viral load; conversely, low intrahepatic IL10 mRNA expression showed a negative association with fibrosis progression. Intrahepatic TGFB1 mRNA expression was greater in the HCV group than in the control group, and regarding different disease phases, its expression increased as fibrosis evolved to more severe forms.ConclusionIntrahepatic IL10 mRNA expression decreases with persistent fibrosis, probably due to the production of TGF-β1, a potent antimitotic and fibrogenic cytokine. IL10 restricts and decreases the immune response and limits the fibrogenic response; however, a decrease in IL10 favors persistent inflammatory infiltrate, resulting in severe fibrosis.
Highlights
Liver fibrosis is a result of continuous damage to the liver combined with accumulation of the extracellular matrix and is characteristic of most chronic liver diseases such as hepatitis C virus (HCV) infection
High intrahepatic interleukin 10 (IL10) mRNA expression showed a positive association with F0-F1 fibrosis, no inflammation, low concentrations of liver enzymes and a high viral load; low intrahepatic IL10 mRNA expression showed a negative association with fibrosis progression
Intrahepatic TGFB1 mRNA expression was greater in the HCV group than in the control group, and regarding different disease phases, its expression increased as fibrosis evolved to more severe forms
Summary
Liver fibrosis is a result of continuous damage to the liver combined with accumulation of the extracellular matrix and is characteristic of most chronic liver diseases such as hepatitis C virus (HCV) infection. Liver fibrosis is a result of chronic damage to the liver combined with extracellular matrix accumulation and is characteristic of most types of chronic liver disease. The cytokines IL-10 and TGF-β1 contribute to an immunotolerant state of the liver, as they inhibit the differentiation of dendritic cells and promote the conversion of naïve CD4 + T cells into regulatory T cells [2, 3]. TGF-β1 is the main cytokine mediator of tissue repair, inducing myofibroblast differentiation, formation of the extracellular matrix, proliferation of fibroblasts and collagen synthesis [4]
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