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"Liver-on-a-Chip" Cultures of Primary Hepatocytes and Kupffer Cells for Hepatitis B Virus Infection
10:25

"Liver-on-a-Chip" Cultures of Primary Hepatocytes and Kupffer Cells for Hepatitis B Virus Infection

Published on: February 19, 2019

Hepatic expression of intercellular adhesion molecule-1 (ICAM-1) in viral hepatitis B

R Volpes1, J J van den Oord, V J Desmet

  • 1Department of Pathology, University Hospital St. Rafaël, Catholic University of Leuven, Belgium.

Hepatology (Baltimore, Md.)
|July 1, 1990
PubMed

Insights

Hepatitis B virus infection alters intercellular adhesion molecule-1 and human leukocyte antigen-DR expression in liver cells. These changes correlate with inflammation severity and viral activity in chronic hepatitis B.

Area of Science:

  • Immunology
  • Hepatology
  • Virology

Background:

  • Intercellular adhesion molecule-1 (ICAM-1) and human leukocyte antigen-DR (HLA-DR) are key immune molecules.
  • Their role in hepatitis B virus (HBV) infection pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the in situ distribution of ICAM-1 and HLA-DR in liver biopsies from HBV-infected patients.
  • To analyze the relationship between viral antigen display (HBcAg) and ICAM-1 expression on hepatocytes.

Main Methods:

  • Immunohistochemical techniques were used on 61 liver biopsy specimens.
  • Double-staining was performed on 14 selected samples to analyze HBcAg and ICAM-1 coexpression.
  • Analysis focused on the correlation with inflammatory infiltrate composition.

Main Results:

  • ICAM-1 and HLA-DR expression on hepatocytes correlated positively with inflammatory infiltrate extent and site.
  • Healthy carriers showed no expression; acute hepatitis displayed strong, widespread expression.
  • Chronic hepatitis and cirrhosis showed focal expression on hepatocytes near inflammation.

Conclusions:

  • ICAM-1 and HLA-DR expression patterns in hepatocytes reflect the inflammatory response in HBV infection.
  • These molecules may play a role in immune cell recruitment and liver damage during chronic hepatitis B.

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