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Hepatic chemerin and chemokine-like receptor 1 expression in patients with chronic hepatitis C
Michał Kukla1, Brygida Adamek2, Marek Waluga1
1Department of Gastroenterology and Hepatology, Medical University of Silesia, Ulica Medyków 14, 40-752 Katowice, Poland.
Insights
This study found chemerin and its receptor CMKLR1 are expressed in the liver of chronic hepatitis C patients. Serum chemerin levels negatively correlated with hepatic chemerin expression.
Area of Science:
- Hepatology
- Immunology
- Molecular Biology
Background:
- Chemerin is implicated in chronic hepatitis C (CHC) pathogenesis.
- Hepatic expression of chemerin and its receptor, chemokine receptor-like 1 (CMKLR1), in CHC remains uninvestigated.
Purpose of the Study:
- To assess hepatic expression of chemerin and CMKLR1 in CHC patients.
- To measure serum chemerin concentrations in CHC patients.
- To correlate these with metabolic and histopathological factors.
Main Methods:
- Quantitative real-time PCR for hepatic chemerin and CMKLR1 mRNA transcription.
- Enzyme-linked immunosorbent assay for serum chemerin.
- Study included 63 nonobese CHC patients.
Main Results:
- Chemerin and CMKLR1 expression was detected in the livers of all CHC patients.
- Hepatic expression did not correlate with necroinflammation, steatosis, fibrosis, or metabolic abnormalities.
- A negative association was observed between serum chemerin and hepatic chemerin expression (r = -0.41, P = 0.006).
Conclusions:
- This study provides the first evidence of significant chemerin and CMKLR1 expression in the CHC liver.
- The primary source of hepatic chemerin and CMKLR1 mRNA (hepatocytes vs. other cells) requires further investigation.
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 (r = (-0.41), P = 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.
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