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A Standardized Method for the Analysis of Liver Sinusoidal Endothelial Cells and Their Fenestrations by Scanning Electron Microscopy
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Mechanism of neutrophil accumulation in sinusoids after extrahepatic biliary obstruction

Yasuo Wakabayashi1, Hiroaki Shimizu, Fumio Kimura

  • 1Department of General Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.

Hepato-Gastroenterology
|September 18, 2008
PubMed
Abstract

Insights

In cholestatic liver injury, endotoxin activates Kupffer cells to produce IL-1beta, increasing CINC release from hepatocytes and leading to neutrophil infiltration.

Area of Science:

  • Hepatology
  • Immunology
  • Gastroenterology

Background:

  • Polymorphonuclear neutrophil (PMN) infiltration is implicated in liver injury.
  • Mechanisms of PMN infiltration in cholestatic liver disease remain unclear.

Purpose of the Study:

  • Investigate PMN infiltration and cytokine-induced neutrophil chemoattractant (CINC) expression in cholestatic liver.
  • Elucidate the role of Kupffer cells and endotoxemia in this process.

Main Methods:

  • Bile duct ligation model in rats to induce cholestasis.
  • Assessed hepatic CINC mRNA, PMN infiltration, and portal venous endotoxin levels.
  • In vitro studies on CINC production by isolated liver cells.

Main Results:

  • Cholestatic livers showed increased PMN infiltration and CINC mRNA expression.
  • Hepatocytes were the primary source of CINC.
  • IL-1beta enhanced CINC production in hepatocytes from cholestatic livers.
  • Kupffer cells from cholestatic livers produced more IL-1beta when stimulated.

Conclusions:

  • Portal endotoxemia in cholestasis activates Kupffer cells.
  • Activated Kupffer cells overproduce IL-1beta.
  • This IL-1beta drives increased CINC release from hepatocytes.
  • The CINC increase promotes PMN infiltration in cholestatic liver injury.

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