BACKGROUND AND AIMS: Recent studies highlight the role of chemokines for the attraction of inflammatory cells in liver injury and fibrogenesis. The CC chemokine ligand 11, eotaxin (CCL11), is up-regulated in senescent human hepatic stellate cells and crucial in animal models of T-cell mediated hepatitis. The aim of this study was to analyze the role of eotaxin in chronic liver disease. METHODS: Plasma eotaxin levels of 111 patients with chronic liver disease were correlated with clinical presentation, laboratory parameters, liver histology and clinical course in a 6-year follow-up. RESULTS: Eotaxin concentrations were significantly up-regulated in patients with liver cirrhosis and increased according to Child-Pugh and model of end-stage liver disease (MELD) score. Eotaxin correlated with the hepatic biosynthetic capacity and other inflammatory cytokines. High eotaxin was associated with hepatic necroinflammation and fibrosis in liver histology. In patients with typical clinical complications of cirrhosis, eotaxin was found to be increased. High eotaxin indicated an unfavorable prognosis in 6-year follow-up. CONCLUSIONS: High eotaxin expression may be involved in the pathogenesis of chronic liver diseases. Plasma eotaxin levels correlate with the degree of liver cirrhosis and could serve as an additional biomarker indicating histological hepatic necroinflammation and fibrosis as well as an adverse clinical course.
BACKGROUND AND AIMS: Recent studies highlight the role of chemokines for the attraction of inflammatory cells in liver injury and fibrogenesis. The CC chemokine ligand 11, eotaxin (CCL11), is up-regulated in senescent human hepatic stellate cells and crucial in animal models of T-cell mediated hepatitis. The aim of this study was to analyze the role of eotaxin in chronic liver disease. METHODS: Plasma eotaxin levels of 111 patients with chronic liver disease were correlated with clinical presentation, laboratory parameters, liver histology and clinical course in a 6-year follow-up. RESULTS:Eotaxin concentrations were significantly up-regulated in patients with liver cirrhosis and increased according to Child-Pugh and model of end-stage liver disease (MELD) score. Eotaxin correlated with the hepatic biosynthetic capacity and other inflammatory cytokines. High eotaxin was associated with hepatic necroinflammation and fibrosis in liver histology. In patients with typical clinical complications of cirrhosis, eotaxin was found to be increased. High eotaxin indicated an unfavorable prognosis in 6-year follow-up. CONCLUSIONS: High eotaxin expression may be involved in the pathogenesis of chronic liver diseases. Plasma eotaxin levels correlate with the degree of liver cirrhosis and could serve as an additional biomarker indicating histological hepatic necroinflammation and fibrosis as well as an adverse clinical course.
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