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Updated: Jun 21, 2026

"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

Electron microscopic alterations in intermediate hepatocyte-like cells in children with chronic hepatitis B: the

Joanna M Lotowska1, Maria E Sobaniec-Lotowska, Dariusz M Lebensztejn

  • 1Departments of General Pathomorphology, Medical University of Bialystok, Poland.

European Journal of Gastroenterology & Hepatology
|July 23, 2009
PubMed

Insights

Chronic hepatitis B in children with fibrosis may promote degenerating intermediate hepatocyte-like cells (IHCs) toward cancer. This ultrastructural study reveals IHC damage linked to fibrosis in pediatric chronic hepatitis B patients.

Area of Science:

  • Hepatology
  • Cell Biology
  • Virology

Background:

  • Chronic hepatitis B viral (HBV) infection is a significant global health concern.
  • Liver progenitor/oval cells, including intermediate hepatocyte-like cells (IHCs), play a role in liver regeneration and disease.
  • Understanding cellular changes in pediatric chronic HBV is crucial for long-term outcomes.

Purpose of the Study:

  • To perform an in-depth ultrastructural analysis of intermediate hepatocyte-like cells (IHCs).
  • To investigate the changes in IHCs in children with chronic hepatitis B viral (HBV) infection.
  • To correlate IHC ultrastructural alterations with liver fibrosis severity.

Main Methods:

  • Ultrastructural investigation using transmission electron microscopy.
  • Analysis of liver biopsy samples from 40 children (aged 3-16 years) with chronic hepatitis B.
  • Sample preparation involved fixation in glutaraldehyde, paraformaldehyde, and cacodylate buffer.

Main Results:

  • Identified IHCs with significant ultrastructural changes, including degeneration, particularly in patients with advanced liver fibrosis.
  • Observed abnormalities in mitochondria (swelling, crest loss, myelin figures) and granular endoplasmic reticulum (shortening, degranulation) within degenerating IHCs.
  • Found primitive phagosome-like structures with biliary pigment and transitional hepatic stellate cells near altered IHCs.

Conclusions:

  • Chronic HBV infection with significant fibrosis in childhood may predispose degenerating IHCs to neoplastic transformation in adulthood.
  • Further research is needed to explore the role of coexisting carcinogenic factors.
  • These findings highlight potential long-term risks associated with pediatric chronic HBV and fibrosis.
Abstract

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