| Changes in blood dendritic cell counts in relation to type of coronary artery disease and brachial endothelial cell function. | |
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MedLine Citation:
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PMID: 20124992 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. CONCLUSION: 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. |
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Authors:
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Emily A Van Vr?; Ilse Van Brussel; Ken Op de Beeck; Vicky Y Hoymans; Christiaan J Vrints; Hidde Bult; Johan M Bosmans |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Coronary artery disease Volume: 21 ISSN: 1473-5830 ISO Abbreviation: Coron. Artery Dis. Publication Date: 2010 Mar |
Date Detail:
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Created Date: 2010-02-12 Completed Date: 2010-04-29 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9011445 Medline TA: Coron Artery Dis Country: England |
Other Details:
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Languages: eng Pagination: 87-96 Citation Subset: IM |
Affiliation:
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Department of Cardiology, University of Antwerp, B-2610 Wilrijk, Belgium. emily@vanvre.be |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic beta-Antagonists
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therapeutic use Aged Brachial Artery / drug effects, physiopathology*, ultrasonography Coronary Angiography Coronary Stenosis / blood*, drug therapy, physiopathology, radiography Dendritic Cells* / drug effects, immunology Endothelium, Vascular / drug effects, physiopathology*, ultrasonography Female Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use Immunophenotyping Inflammation Mediators / blood Leukocyte Count Male Middle Aged Severity of Illness Index Vasodilation* / drug effects |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic beta-Antagonists; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0/Inflammation Mediators |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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