title: Phagocytic and oxidative burst activity of neutrophils in the end stage of liver cirrhosis.
abstract: OBJECTIVE
  To evaluate the phagocytic activity and neutrophil oxidative burst in liver cirrhosis.
  
  
  METHODS
  In 45 patients with advanced postalcoholic liver cirrhosis (aged 45+/-14 years) and in 25 healthy volunteers (aged 38+/-5 years), the percentage of phagocytizing cells after in vitro incubation with E. coli (Phagotest Kit), phagocytic activity (mean intensity of fluorescence, MIF) and the percentage of neutrophil oxidative burst (Bursttest Kit), and the level of free oxygen radical production (MIF of Rodamine 123) were analyzed by flow cytometry. The levels of soluble sICAM-1, sVCAM-1, sP-selectin, sE-selectin, sL-selectin, and TNF-alpha were determined in blood serum.
  
  
  RESULTS
  The percentage of E. coli phagocytizing neutrophils in liver cirrhosis patients was comparable to that in healthy subjects. MIF of neutrophil -- ingested E. coli was higher in patients with liver cirrhosis. The oxidative burst in E. coli phagocytizing neutrophils generated less amount of active oxygen compounds in liver cirrhosis patients (MIF of R123: 24.7+/-7.1 and 29.7+/-6.6 in healthy, P<0.01). Phorbol myristate acetate (PMA) -- stimulated neutrophilsproduced less reactive oxidants in liver cirrhosis patients than in healthy subjects (MIF of R123: 42.7+/-14.6 vs 50.2+/-13.3, P<0.01). A negative correlation was observed between oxidative burst MIF of PMA-stimulated neutrophils and ALT and AST levels (r -0.35, P<0.05; r-0.4, P<0.03). sVCAM-1, sICAM-1, sE-selectin concentrations correlated negatively with the oxygen free radical production (MIF of R123) in neutrophils after PMA stimulation in liver cirrhosis patients (r-0.45, P<0.05; r-0.41, P<0.05; r-0.39, P<0.05, respectively).
  
  
  CONCLUSIONS
  Neutrophil metabolic activity diminishes together with the intensification of liver failure. The metabolic potential of phagocytizing neutrophils is significantly lower in liver cirrhosis patients, which can be one of the causes of immune mechanism damage. The evaluation of oxygen metabolism of E. coli-stimulated neutrophils reveals that the amount of released oxygen metabolites is smaller in liver cirrhosis patients than in healthy subjects.
authors.affiliation: Department of Infectious Diseases, Medical University of Bialystok, Zurawia Str, 14, 15-540 Bialystok, Poland. anatol@panasiuk.pl
authors.forename: Anatol
authors.initials: A
authors.lastname: Panasiuk
authors.forename: Jolanta
authors.initials: J
authors.lastname: Wysocka
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Maciorkowska
authors.forename: Bozena
authors.initials: B
authors.lastname: Panasiuk
authors.forename: Danuta
authors.initials: D
authors.lastname: Prokopowicz
authors.forename: Janusz
authors.initials: J
authors.lastname: Zak
authors.forename: Karol
authors.initials: K
authors.lastname: Radomski
mesh_terms: D000328:Adult; D019040:E-Selectin / Q000097:blood; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008103:Liver Cirrhosis / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism; D010587:Phagocytosis; D016897:Respiratory Burst; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D019040:E-Selectin; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1