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• W2043291497 abstract "To the Editor: In their review,1 Gao and colleagues discuss possible underlying mechanisms related to host factor involvement in interferon (IFN)-alpha treatment failure. Although comprehensive, the review failed to point out the key role of cholestasis and bile salts in ailing innate and acquired immunity as well as IFN-alpha signaling in the liver. During the last 2 decades, it has been repeatedly shown that cholestasis suppresses allogenic responses and immune-mediated pathologies.2-4 Consistent with these observations, we demonstrated that bile acids at concentrations found in the blood and liver in chronic liver diseases exhibit immunosuppressive properties5 and markedly inhibit IFN-induced antiviral proteins.6 In further experiments using CHO cells stably expressing a human bile acid carrier, we found that bile acid inhibition of the IFN pathway occurred in the range of 10- to 50-μmol concentrations.7 We also provided evidence that the molecular mechanism involved a trans-suppressor effect of bile acids on IFN-responsive gene expression. (STAT)s thyrosine phosphorylation was not modified, while IFN-induced MxA promoter activity was markedly reduced. All of these data are consistent with the high replication rate of hepatitis B and hepatitis C viruses in the context of severe and progressive cholestasis after liver transplantation. In human studies we found that indirect indicators of cholestasis (serum activity of gamma glutamyl transpeptidase, or extensive fibrosis or cirrhosis) were predictors of failure of IFN treatment in hepatitis C virus infection.8 Subsequently, we designed a controlled trial aimed at assessing the potential of ursodeoxycholic acid to restore IFN sensitivity in hepatitis C virus infection, postulating that ursodeoxycholic acid could counteract the inhibitory effects of endogenous bile acids and subclinical cholestasis.9 Indeed, in vitro ursodeoxycholic has no or minimal effect on the IFN-signaling pathway. This trial failed to show a significant benefit in terms of sustained negativation of hepatitis C viremia in ursodeoxycholic acid–treated patients. In contrast to what occurs in chronic cholestatic disorders, ursodeoxycholic acid was unable to produce significant changes in serum bile acid levels and composition in this study, thus providing a plausible explanation for its lack of antiviral property in vivo. We hope that this additional information will be useful and will bolster the knowledge of young investigators in the field of “bile-ology.” Raoul Poupon M.D.*, * Service d'Hepatologie, Hopital Saint-Antoine, AP-Hopîtaux de Paris, Paris, France." @default.
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• W2043291497 date "2004-01-01" @default.
• W2043291497 modified "2023-09-27" @default.
• W2043291497 title "Cholestasis and failure of interferon-alpha treatment" @default.
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• W2043291497 doi "https://doi.org/10.1002/hep.20343" @default.
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