title: Heterogeneity of peripheral blood monocytes, endothelial dysfunction and subclinical atherosclerosis in patients with systemic lupus erythematosus.
abstract: BACKGROUND
  Systemic lupus erythematosus (SLE) is characterized by increased cardiovascular morbidity and mortality. SLE patients have increased prevalence of subclinical atherosclerosis, although the mechanisms of this observation remain unclear. Considering the emerging role of monocytes in atherosclerosis, we aimed to investigate the relationship between subclinical atherosclerosis, endothelial dysfunction and the phenotype of peripheral blood monocytes in SLE patients.
  
  
  METHODS
  We characterized the phenotype of monocyte subsets defined by the expression of CD14 and CD16 in 42 patients with SLE and 42 non-SLE controls. Using ultrasonography, intima-media thickness (IMT) of carotid arteries and brachial artery flow-mediated dilation (FMD) as well as nitroglycerin-induced dilation (NMD) were assessed.
  
  
  RESULTS
  Patients with SLE had significantly, but only modestly, increased IMT when compared with non-SLE controls (median (25th/75th percentile) 0.65 (0.60/0.71) mm vs 0.60 (0.56/0.68) mm; p < 0.05). Importantly, in spite of early atherosclerotic complications in the studied SLE group, marked endothelial dysfunction was observed. CD14dimCD16+proinflammatory cell subpopulation was positively correlated with IMT in SLE patients. This phenomenon was not observed in control individuals. Interestingly, endothelial dysfunction assessed by FMD was not correlated with any of the studied monocyte subsets.
  
  
  CONCLUSIONS
  Our observations suggest that CD14dimCD16+monocytes are associated with subclinical atherosclerosis in SLE, although the mechanism appears to be independent of endothelial dysfunction.
authors.affiliation: Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland.
authors.forename: T P
authors.initials: TP
authors.lastname: Mikołajczyk
authors.affiliation: Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland.
authors.forename: G
authors.initials: G
authors.lastname: Osmenda
authors.affiliation: Division of Rheumatology, J Dietl Clinical Hospital, Krakow, Poland.
authors.forename: B
authors.initials: B
authors.lastname: Batko
authors.affiliation: Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland.
authors.forename: G
authors.initials: G
authors.lastname: Wilk
authors.affiliation: Division of Rheumatology, J Dietl Clinical Hospital, Krakow, Poland.
authors.forename: M
authors.initials: M
authors.lastname: Krezelok
authors.affiliation: Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland Institute of Cardiovascular and Medical Sciences, University of Glasgow, UK.
authors.forename: D
authors.initials: D
authors.lastname: Skiba
authors.affiliation: Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland.
authors.forename: T
authors.initials: T
authors.lastname: Sliwa
authors.affiliation: Department of Immunology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.
authors.forename: J R
authors.initials: JR
authors.lastname: Pryjma
authors.affiliation: Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland Institute of Cardiovascular and Medical Sciences, University of Glasgow, UK t.guzik@uj.edu.pl.
authors.forename: T J
authors.initials: TJ
authors.lastname: Guzik
mesh_terms: D000328:Adult; D000368:Aged; D058070:Asymptomatic Diseases; D050197:Atherosclerosis / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology*; D059168:Carotid Intima-Media Thickness; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005434:Flow Cytometry; D058851:GPI-Linked Proteins / Q000097:blood; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000097:blood*; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000150:complications* / Q000175:diagnosis; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D010641:Phenotype; D011237:Predictive Value of Tests; D017452:Receptors, IgG / Q000097:blood*; D012307:Risk Factors; D014664:Vasodilation; D055815:Young Adult
chemical_list: D015415:Biomarkers; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018950:Lipopolysaccharide Receptors; D017452:Receptors, IgG
keywords: Intima-media thickness; SLE; flow-mediated dilation; monocyte subsets