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Open AccessArticle

Elevated Levels of Endocannabinoids in Chronic Hepatitis C May Modulate Cellular Immune Response and Hepatic Stellate Cell Activation

1
Department of Clinical Research, University of Bern, Bern 3010, Switzerland
2
Institute of Biochemistry and Molecular Medicine, University of Bern, Bern 3012, Switzerland
3
Department of Clinical Research, Laboratory of Phytopharmacology, Bioanalytics and Pharmacokinetics, University of Bern, Bern 3010, Switzerland
4
Department of Visceral Surgery and Medicine, Inselspital, University of Bern, Bern 3010, Switzerland
5
Department of Nephrology, Inselspital, University of Bern, Bern 3010, Switzerland
6
Department of Medicine II, Division of Gastroenterology, University of Dresden, Dresden 01307, Germany
7
Department of Visceral Surgery, University of Schleswig-Holstein, Campus Kiel, Kiel 24105, Germany
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Tatsuo Kanda
Int. J. Mol. Sci. 2015, 16(4), 7057-7076; https://doi.org/10.3390/ijms16047057
Received: 20 January 2015 / Revised: 6 March 2015 / Accepted: 23 March 2015 / Published: 27 March 2015
(This article belongs to the Special Issue Viral Hepatitis Research)
The endocannabinoid (EC) system is implicated in many chronic liver diseases, including hepatitis C viral (HCV) infection. Cannabis consumption is associated with fibrosis progression in patients with chronic hepatitis C (CHC), however, the role of ECs in the development of CHC has never been explored. To study this question, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) were quantified in samples of HCV patients and healthy controls by gas and liquid chromatography mass spectrometry. Fatty acid amide hydrolase (FAAH) and monoaclyglycerol lipase (MAGL) activity was assessed by [3H]AEA and [3H]2-AG hydrolysis, respectively. Gene expression and cytokine release were assayed by TaqMan PCR and ELISpot, respectively. AEA and 2-AG levels were increased in plasma of HCV patients, but not in liver tissues. Hepatic FAAH and MAGL activity was not changed. In peripheral blood mononuclear cells (PBMC), ECs inhibited IFN-γ, TNF-α, and IL-2 secretion. Inhibition of IL-2 by endogenous AEA was stronger in PBMC from HCV patients. In hepatocytes, 2-AG induced the expression of IL-6, -17A, -32 and COX-2, and enhanced activation of hepatic stellate cells (HSC) co-cultivated with PBMC from subjects with CHC. In conclusion, ECs are increased in plasma of patients with CHC and might reveal immunosuppressive and profibrogenic effects. View Full-Text
Keywords: endocannabinoid system; hepatitis C; peripheral blood mononuclear cells; inflammation; fibrosis; liver endocannabinoid system; hepatitis C; peripheral blood mononuclear cells; inflammation; fibrosis; liver
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Patsenker, E.; Sachse, P.; Chicca, A.; Gachet, M.S.; Schneider, V.; Mattsson, J.; Lanz, C.; Worni, M.; De Gottardi, A.; Semmo, M.; Hampe, J.; Schafmayer, C.; Brenneisen, R.; Gertsch, J.; Stickel, F.; Semmo, N. Elevated Levels of Endocannabinoids in Chronic Hepatitis C May Modulate Cellular Immune Response and Hepatic Stellate Cell Activation. Int. J. Mol. Sci. 2015, 16, 7057-7076.

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