Keywords : CCR2
European Journal of Molecular & Clinical Medicine,
2020, Volume 7, Issue 11, Pages 6071-6082
Background: Collagen producing myofibroblast activation of is critical for pathogenesis of liver fibrosis. Aim of the work: To study the expansion of peripheral monocyte subsets in HCV patients. Subjects and Methods: Sixty HCV patients were classified according to METAVIR score into 4 stages of liver fibrosis, 15 age and sex-matched controls were include. Flowcytometric analysis of peripheral blood monocytes subsets and CCR2+ve cells was
carried out using monoclonal anti-CD45, anti-CD14, anti-CD16, anti-collagen type I and anti-CCR2antibodies. MCP-1 and SAP levels were assessed using ELISA. Results and Conclusions: A down regulation (p< 0.01) in the classical monocytes subset and an up regulation (p< 0.01) in both the non-classical monocytes and monocytes
producing collagen subsets were notice in HCV patients compared to controls. A marked increase (p< 0.01) in the levels of MCP-1 and monocytes expressing CCR2 with a significant decrease (p< 0.01) in SAP levels, which paralleled the progression of liver fibrosis, were also noticed. MCP-1 and CCR2 may trigger monocytes recruitment to the injured liver promoting the development of collagen type I producing monocytes. The shift
of classical monocyte subset towards the non-classical and collagen producing subsets may be present a predictive non-invasive biomarkers for progress of liver fibrosis.