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Hepatitis B virus X protein induced expression of interleukin 18: a potential mechanism for liver injury caused by hepatitis B virus (HBV) infection

Authors
 Mi Ock Lee  ;  Youn Hee Choi  ;  Eui Cheol Shin  ;  Hyo Jin Kang  ;  Young Mee Kim  ;  Su Yon Jeong  ;  Je Kyung Seong  ;  Dae Yeul Yu  ;  Hyeseong Cho  ;  Jeon Han Park  ;  Se Jong Kim 
Citation
 JOURNAL OF HEPATOLOGY, Vol.37(3) : 380-386, 2002 
Journal Title
 JOURNAL OF HEPATOLOGY 
ISSN
 0168-8278 
Issue Date
2002
MeSH
Animals ; Carcinoma, Hepatocellular ; Fas Ligand Protein ; Gene Expression Regulation, Viral ; Hepatitis B virus/physiology* ; Hepatitis B, Chronic/immunology* ; Hepatitis B, Chronic/pathology ; Hepatitis B, Chronic/virology* ; Hepatocytes/immunology ; Hepatocytes/pathology ; Hepatocytes/virology ; Humans ; Interleukin-18/genetics* ; Interleukin-18/metabolism ; Liver/immunology ; Liver/pathology ; Liver/virology ; Liver Neoplasms ; Membrane Glycoproteins/genetics ; Mice ; Mice, Transgenic ; Trans-Activators/genetics* ; Transcription, Genetic/physiology ; Tumor Cells, Cultured
Keywords
Hepatitis B virus X protein ; Interleukin 18 ; Fas ligand ; Liver injury
Abstract
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.
Full Text
http://www.sciencedirect.com/science/article/pii/S0168827802001812
DOI
10.1016/S0168-8278(02)00181-2
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Se Jong(김세종)
Park, Jeon Han(박전한) ORCID logo https://orcid.org/0000-0001-9604-3205
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/143625
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