title: Neutrophils obtained from obliterative atherosclerotic patients exhibit enhanced resting respiratory burst and increased degranulation in response to various stimuli.
abstract: Tissue destruction in atherosclerosis is partly due to uncontrolled protease and oxygen radical release. In this study we investigated the release of elastase and myeloperoxidase, as well as the production of reactive oxygen species by polymorphonuclear leukocytes (PMNLs) obtained from patients with obliterative atherosclerotic of the lower legs. In addition we measured the plasma concentration of xanthine oxidase. PMNLs of atherosclerotic patients have a greater ability to increase elastase and myeloperoxidase release after their stimulation with formyl-methionin-leucyl-phenylalanin (fMLP) and calcium ionophore, A23187, independently of their age, than PMNLs of healthy middle-aged subjects. Similarly to healthy elderly subjects there was an increased superoxide anion (O2-) production under basal condition in both atherosclerotic patient age-groups. The activation of PMNLs with fMLP and A23187 enhanced O2- formation both in healthy subjects and in patients with atherosclerotic disease of the lower legs, however the increase was significantly less in the latter group. No biochemical parameters showed significant correlation with patient's risk factors, however myeloperoxidase production was significantly higher in less severe stage of the disease (P < 0.05). We found that patients with atherosclerotic disease of the lower legs have higher plasma xanthine oxidase level than control subjects. This study indicates an other piece of evidence suggesting the activation and involvement of neutrophils in the pathogenesis of atherosclerosis of the lower legs. The similar tendencies in the reactivity of neutrophils during aging and in atherosclerosis suggest that atherosclerosis may be an early aging process.
authors.affiliation: First Department of Medicine, University Medical School of Debrecen, Hungary. mohacsi@ibel-dote.hu
authors.forename: A
authors.initials: A
authors.lastname: Mohàcsi
authors.forename: B
authors.initials: B
authors.lastname: Kozlovszky
authors.forename: I
authors.initials: I
authors.lastname: Kiss
authors.forename: I
authors.initials: I
authors.lastname: Seres
authors.forename: T
authors.initials: T
authors.lastname: Fülöp
mesh_terms: D000328:Adult; D000368:Aged; D001161:Arteriosclerosis / Q000378:metabolism*; D000001:Calcimycin / Q000494:pharmacology; D015550:Cell Degranulation; D004549:Elastin / Q000494:pharmacology; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D007476:Ionophores / Q000494:pharmacology; D019272:Leukocyte Elastase; D008875:Middle Aged; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000378:metabolism*; D010196:Pancreatic Elastase / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D016897:Respiratory Burst; D013481:Superoxides / Q000378:metabolism; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D007476:Ionophores; D013481:Superoxides; D000001:Calcimycin; D009240:N-Formylmethionine Leucyl-Phenylalanine; D004549:Elastin; D006861:Hydrogen Peroxide; D009195:Peroxidase; D014969:Xanthine Oxidase; D010196:Pancreatic Elastase; D019272:Leukocyte Elastase