Open AccessInduction of intercellular adhesion molecule‐1 (CD54) on human hepatoma cell line HepG2: influence of cytokines and hepatitis B virus‐DNA transfection
Author(s) -
VOLPES R.,
OORD J. J.,
DESMET V. J.,
YAP S.H.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb06415.x
Subject(s) - intercellular adhesion molecule 1 , transfection , cell adhesion molecule , biology , microbiology and biotechnology , hepatitis b virus , cytokine , cell culture , virology , virus , immunology , genetics
SUMMARY Human hepatocyte expression of intercellular adhesion molecule‐1 (ICAM‐1)(CD54) was studied in vitro by exposing the well differentiated human hepatoblastoma cell line HepG2 to various cytokines. In addition, hepatitis B virus (HBV)‐DNA transfected HepG2 cells were also analysed. Expression of ICAM‐1 on HepG2 cells was then revealed with an immunohistochemical procedure. Untreated HepG2 cells were unreactive, but showed strong cytoplasmic ICAM‐1 immunoreactivity after treatment with interferon‐gamma (IFN‐γ). This induction was completely inhibited by addition of a neutralizing antibody directed to IFN‐γ, IL‐1, IL‐6, tumour necrosis factor‐α (TNF‐α) and IFN‐α used alone or in combination, did not induce ICAM‐1 expression, neither did they inhibit the IFN‐γ‐induced expression of this adhesion molecule on HepG2 cells. Untreated hepatitis B virus‐DNA transfected HepG2 cells expressed membranous ICAM‐1. These results indicate that IFN‐γ is the main cytokine trigger for ICAM‐1 expression on HepG2 cells, suggesting that in areas of liver inflammation this adhesion molecule is up‐regulated on hepatocytes by locally released IFN‐γ. In addition, expression of ICAM‐1 by hepatitis B virus‐DNA transfected HepG2 cells suggests other, still unknown, triggering mechanisms in the induction of such adhesion molecules, for instance gene activation by viral genome, or autocrine virus‐induced hepatocellular cytokine production.