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BioMed Research International
Volume 2014, Article ID 517820, 12 pages
http://dx.doi.org/10.1155/2014/517820
Research Article

Hepatic Chemerin and Chemokine-Like Receptor 1 Expression in Patients with Chronic Hepatitis C

1Department of Gastroenterology and Hepatology, Medical University of Silesia, Ulica Medyków 14, 40-752 Katowice, Poland
2Department of General Biology, Medical University of Silesia, Katowice, Poland
3Department of Environmental Medicine and Epidemiology, Medical University of Silesia, Katowice, Poland
4Department of Pathomorphology in Zabrze, Medical University of Silesia, Katowice, Poland
5Department of Infectious Diseases in Chorzów, Medical University of Silesia, Katowice, Poland
6Department of Infectious Diseases in Bytom, Medical University of Silesia, Katowice, Poland
7Department of Physiology in Zabrze, Medical University of Silesia, Katowice, Poland
8Department of Paediatrics in Zabrze, Medical University of Silesia, Katowice, Poland

Received 28 February 2014; Revised 15 June 2014; Accepted 17 June 2014; Published 10 July 2014

Academic Editor: Jun Yong Park

Copyright © 2014 Michał Kukla et al. 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.

Abstract

Introduction. Chemerin seems to be involved in pathogenesis of chronic hepatitis C (CHC). Hepatic expressions of chemerin and its receptor, chemokine receptor-like 1 (CMKLR1), in CHC have not been studied so far. Aim. To evaluate chemerin and CMKLR1 hepatic expression together with serum chemerin concentration in CHC patients and to assess their relationship with metabolic and histopathological abnormalities. Methods. The study included 63 nonobese CHC patients. Transcription of chemerin and CMKLR1 was assessed by quantitative real-time PCR, while serum chemerin was assessed by enzyme-linked immunosorbent assay. Results. Expression of chemerin and CMKLR1 was present in the liver of all CHC patients regardless of sex or age. This expression was not associated with necroinflammatory activity and steatosis grade, fibrosis stage, and metabolic abnormalities. There was a negative association between serum chemerin and chemerin hepatic expression ( = (−0.41), = 0.006). Conclusion. The study for the first time confirmed a marked expression of chemerin and CMKLR1 in the liver of CHC patients. The study was performed using the homogenates of human liver tissue, so it is not possible to define whether hepatocytes or other cell types which are abundantly represented in the liver constitute the main source of chemerin and CMKLR1 mRNA.