title: Changes in blood dendritic cell counts in relation to type of coronary artery disease and brachial endothelial cell function.
abstract: BACKGROUND
  Recently we reported a decline of circulating myeloid (m) and plasmacytoid (p) dendritic cells (DCs) in patients with coronary artery disease (CAD). This study also determined the total blood DC numbers and focused on effects of extent (one vs. three-vessel disease) and type (stable vs. unstable) of CAD, and on endothelial cell function.
  
  
  METHODS
  Patients undergoing diagnostic coronarography were enrolled in four groups: control patients (atypical chest pain, <50% narrowing, n=15), stable one-vessel (n=15), stable three-vessel (n=15), and unstable one-vessel CAD (n=16). Total blood DCs were identified as lineage (lin) and HLADR, and DC subtypes with blood DC antigen (BDCA)-1 for mDCs and BDCA-2 for pDCs. Flow-mediated dilatation (FMD) was measured in the brachial artery.
  
  
  RESULTS
  Numbers of total blood DCs, mDCs and pDCs declined in CAD patients compared with control patients, but without differences between the CAD groups. Interleukin-6 and high sensitivity C-reactive protein displayed inverse associations with mDCs. A FMD below the median of the study population, use of beta-blockers or of lipid-lowering drugs was associated with increased mDCs, whereas pDCs were similar. Interestingly, the effects of drugs and FMD were additive with that of CAD.
  
  
  CONCLUSIONS
  This study indicates that lower blood DCs do not result from medication intake or endothelial dysfunction, and are an overall systemic effect of atherosclerosis rather than CAD type (stable or unstable) or number of stenotic coronary arteries. In view of discrete associations with cytokines, FMD, beta-blockers and statins, mDCs and pDCs seem to behave differently and may influence inflammation during atherosclerosis in different ways.
authors.affiliation: Department of Cardiology, University of Antwerp, B-2610 Wilrijk, Belgium. emily@vanvre.be
authors.forename: Emily A
authors.initials: EA
authors.lastname: Van Vré
authors.forename: Ilse
authors.initials: I
authors.lastname: Van Brussel
authors.forename: Ken Op
authors.initials: KO
authors.lastname: de Beeck
authors.forename: Vicky Y
authors.initials: VY
authors.lastname: Hoymans
authors.forename: Christiaan J
authors.initials: CJ
authors.lastname: Vrints
authors.forename: Hidde
authors.initials: H
authors.lastname: Bult
authors.forename: Johan M
authors.initials: JM
authors.lastname: Bosmans
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology*; D017023:Coronary Angiography; D023921:Coronary Stenosis / Q000097:blood* / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D016130:Immunophenotyping; D018836:Inflammation Mediators / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D014463:Ultrasonography; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000319:Adrenergic beta-Antagonists; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators