The role of monocyte chemoattractant protein-1 in biliary atresia

J Pediatr Surg. 2006 Dec;41(12):1967-72. doi: 10.1016/j.jpedsurg.2006.08.018.

Abstract

Background: The aim of this study was to explain the role of monocyte chemoattractant protein-1 (MCP-1) in biliary atresia (BA).

Methods: Concentrations of serum MCP-1 and collagen type IV were measured in 38 patients with BA by using commercially available kits. MCP-1 was also assessed in liver biopsy specimens by using immunohistochemistry. Subjects were classified into groups. Group 1 comprised BA patients with normal liver function (n = 13), group II comprised BA patients with moderate liver dysfunction (n = 18), group III comprised BA patients older than 20 years awaiting liver transplantation (n = 7), and the control group comprised age-matched patients without evidence of liver disease (n = 23).

Results: Serum MCP-1 levels were significantly increased in group II compared with group I (P < .0001) and the control group (P < .0001). Serum MCP-1 levels in group III were lower than in the control group (P < .0001). There was a significant linear correlation between serum MCP-1 levels and type IV collagen levels in group II. Group II subjects with portal hypertension (PH) had higher MCP-1 levels than those without PH (P = .0009). Biopsy specimens showed MCP-1 was expressed mainly on biliary epithelial cells, vascular endothelial cells, and hepatocytes in group II.

Conclusions: These findings suggest that MCP-1 probably plays a significant role in the development of progressive liver fibrosis in BA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Biliary Atresia / blood
  • Biliary Atresia / complications
  • Biliary Atresia / physiopathology*
  • Chemokine CCL2 / blood*
  • Child
  • Child, Preschool
  • Collagen Type IV / blood
  • Digestive System Surgical Procedures
  • Disease Progression
  • Humans
  • Hypertension, Portal / etiology
  • Hypertension, Portal / physiopathology
  • Liver Cirrhosis / etiology
  • Liver Cirrhosis / physiopathology*
  • Treatment Outcome

Substances

  • Chemokine CCL2
  • Collagen Type IV