Hepatitis B virus X protein induced expression of interleukin 18 (IL-18) : a potential mechanism for liver injury caused by hepatitis B virus (HBV) infection
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- Hepatitis B virus X protein induced expression of interleukin 18 (IL-18) : a potential mechanism for liver injury caused by hepatitis B virus (HBV) infection
- M O Lee; Y H Choi; E C Shin; H J Kang; Y M Kim; S Y Jeong; J K Seong; Dae Yeul Yu; H S Cho; J H Park; S J Kim
- Bibliographic Citation
- Journal of Hepatology, vol. 37, no. 3, pp. 380-386
- Publication Year
- Background/Aims: The hepatitis B virus X protein (HBx), a major viral transactivator, is implicated in hepatic inflammation, since it induces many pro-inflammatory cytokines at transcriptional level. The aim of this study was to investigate role of HBx in expression of interleukin 18 (IL-18), a newly identified cytokine that up-regulates Fas ligand (FasL) expression. Methods: Chang X-34 that expressing HBx under the control of a doxycycline-inducible promoter, and hepatitis B virus (HBV)-integrated hepatoma cell lines were examined for IL-18 expression by Northern and Western blotting analysis. To test the role of IL-18 produced by hepatoma cells, FasL expression was examined by flow cytometry after treatment with neutralizing anti-IL-18 antibodies. Further, IL-18 expression was examined in the liver tissues of HBx-transgenic mice. Results: Induction of IL-18 following HBx expression in Chang X-34 and the pattern of IL-18 expression in HBV-integrated cell lines, implicated that HBx transcriptionally induces IL-18 expression. Neutralizing anti-IL-18 antibodies blocked the expression of FasL, suggesting that IL-18 plays a critical role in FasL expression. Further, IL-18 expression in the HBx-transgenic liver, was correlated with the degree of hepatitis. Conclusions: Our results demonstrated that HBx induces IL-18 expression in liver, which may be associated with hepatic injury by amplifying FasL expression during HBV infection.
- Fas ligandHepatitis B virus X proteinInterleukin 18Liver injury
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