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Mediators of Inflammation
Volume 13 (2004), Issue 5-6, Pages 357-359

Semiquantitative analysis of intrahepatic CC-chemokine mRNAs in chronic hepatitis C

1Department of Internal Medicine I, University of Bonn, Bonn, Germany
2Department of Pathology, University of Bonn, Bonn, Germany

Copyright © 2004 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


BACKGROUND: The mechanisms leading to hepatic injury in chronic hepatitis C virus (HCV) infection are only incompletely understood. Recent data propose a correlation of the intrahepatic expression of the CC chemokine RANTES and the degree of periportal and portal inflammatory liver damage.

Aim: Here, we have studied the intrahepatic mRNA levels of CC chemokines RANTES together with that of other members of this chemokine family (MIP-1β, MCP-1, and MCP-2) in chronic hepatitis C as compared with healthy controls.

Methods: Liver samples from 22 HCV-infected patients, nine individuals with primary biliary cirrhosis and from 12 normal controls were included into this study. Intrahepatic mRNA levels of CC chemokines RANTES, MIP-1β, MCP-1, and MCP-2 were analyzed by a semi-quantitative reverse transcription/real-time polymerase chain reaction assay.

Results: In chronic HCV infection, intrahepatic RANTES mRNA levels were significantly higher than in non-infected controls (7.2-fold, p<0.001) or in the disease control group (2.8-fold, p<0.001) and higher levels of RANTES mRNA levels were observed in livers with an advanced stage of liver cell injury (histologic activity index ≥6), although this difference was not statistically significant (p=0.08). In contrast, mRNA levels of MIP-1β (p=0.021) and MCP-1 (p=0.021) were significantly lower in HCV liver samples while MCP-2 expression was similar in all groups analyzed.

Conclusion: The data support the concept of chemokines as mediators of liver cell injury in chronic hepatitis C.