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Oxygen-derived free radical production by peripheral blood neutrophils in chronic cholestatic liver diseases

A D'Odorico1, A Melis, A Baragiotta

  • 1Department of Surgical and Gastroenterological Sciences, University of Padova, Italy.

Hepato-Gastroenterology
|August 3, 1999
PubMed
Abstract

Insights

In chronic cholestatic liver diseases, neutrophil function remains normal, not explaining increased infection susceptibility. Biohumoral factors may influence neutrophil activation in these patients.

Area of Science:

  • Hepatology
  • Immunology
  • Biochemistry

Background:

  • Patients with chronic cholestasis and cirrhosis face higher risks of infectious complications.
  • Animal models suggest cholestasis impairs polymorphonuclear leukocyte (PMNL) function, impacting immune response.
  • This study investigates neutrophil activity in producing oxygen-derived free radicals in chronic cholestatic liver diseases.

Purpose of the Study:

  • To evaluate neutrophil activity in oxygen-derived free radical production in patients with chronic cholestatic liver diseases.
  • To assess if PMNL function is impaired in primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC).
  • To determine the relationship between liver disease severity, cholestasis degree, and PMNL function.

Main Methods:

  • Included 27 PBC patients, 12 PSC patients, 29 healthy controls, 19 HCV-related cirrhosis patients, and 23 ulcerative colitis patients.
  • Isolated peripheral neutrophils and measured PMNL activity via free radical production using a chemiluminometer.
  • Stimulated neutrophils with fMLP, PMA, and Zymosan to assess response.

Main Results:

  • Both PBC and PSC patients showed normal PMNL activity compared to healthy subjects across all stimuli.
  • In PBC patients, higher disease stage correlated with increased reactive oxygen species (ROS) production.
  • Stage IV PBC patients exhibited significantly higher PMNL activity than HCV-related cirrhotic patients; PSC patients showed no significant differences related to UC.

Conclusions:

  • Impaired PMNL activity does not explain the increased susceptibility to bacterial infections in chronic cholestatic liver disease.
  • Findings suggest that biohumoral factors, potentially cytokines, may influence PMNL activation in these conditions.

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