title: Primed polymorphonuclear leukocytes constitute a possible link between inflammation and oxidative stress in hyperlipidemic patients.
abstract: BACKGROUND
  Oxidative stress (OS) and chronic inflammation are involved and contribute to the development of atherosclerosis. Primed polymorphonuclear leukocytes (PMNLs) are a possible source for superoxide radicals and inflammatory mediators, hence can promote OS and inflammation. The involvement of primed PMNLs in clinical states associated with high risk for developing cardiovascular disease and atherosclerosis, such as hypertension, renal failure and diabetes has been described, however, little is known about PMNLs characteristics in hyperlipidemic patients.
  
  
  METHODS
  Hyperlipidemic patients and healthy control (HC) subjects were enrolled in this cross-sectional study. PMNL priming was estimated by measuring the rate of superoxide release and by levels of membrane CD11b. PMNL priming and myeloperoxidase (MPO) levels served as OS indices. Inflammation was linked to peripheral white blood cells and PMNL counts and to apoptosis. Systemic inflammation was estimated by blood levels of fibrinogen, C-reactive protein (CRP), transferrin and albumin. PMNL priming and inflammation parameters were related to the severity of hyperlipidemia.
  
  
  RESULTS
  PMNLs from hyperlipidemic patients are primed compared to HC. A decrease in PMNL-MPO levels with increased levels of serum MPO were found in hyperlipidemic patients. Leukocyte counts tended to be higher in hyperlipidemic patients with increased PMNL apoptosis. PMNL priming and fibrinogen levels correlated positively with the severity of hyperlipidemia (r=0.32, P=0.02 for CD11b vs. cholesterol and r=0.38, P=0.009 for CD11b vs. LDL-c; r=0.35, P=0.01 for fibrinogen vs. cholesterol and r=0.3, P=0.03 for superoxide release vs. LDL-c).
  
  
  CONCLUSIONS
  PMNLs are primed in hyperlipidemic patients contributing to OS and inflammation in these patients. This study highlights primed PMNLs as an additional risk factor for promoting atherosclerosis in hyperlipidemic patients.
authors.affiliation: Eliachar Research Laboratory, Western Galilee Hospital, Nahariya, Israel.
authors.forename: Rafi
authors.initials: R
authors.lastname: Mazor
authors.forename: Revital
authors.initials: R
authors.lastname: Shurtz-Swirski
authors.forename: Raymond
authors.initials: R
authors.lastname: Farah
authors.forename: Batya
authors.initials: B
authors.lastname: Kristal
authors.forename: Galina
authors.initials: G
authors.lastname: Shapiro
authors.forename: Faina
authors.initials: F
authors.lastname: Dorlechter
authors.forename: Meital
authors.initials: M
authors.lastname: Cohen-Mazor
authors.forename: Edna
authors.initials: E
authors.lastname: Meilin
authors.forename: Snitkovski
authors.initials: S
authors.lastname: Tamara
authors.forename: Shifra
authors.initials: S
authors.lastname: Sela
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism; D000328:Adult; D017209:Apoptosis; D039481:CD11b Antigen / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000276:immunology*; D007249:Inflammation / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology*; D018384:Oxidative Stress / Q000276:immunology*; D009195:Peroxidase / Q000097:blood / Q000378:metabolism; D013481:Superoxides / Q000097:blood / Q000378:metabolism
chemical_list: D000209:Acute-Phase Proteins; D039481:CD11b Antigen; C509295:ITGAM protein, human; D013481:Superoxides; D009195:Peroxidase