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Published on: January 28, 2020
Changes in blood dendritic cell counts in relation to type of coronary artery disease and brachial endothelial cell
Emily A Van Vré1, Ilse Van Brussel, Ken Op de Beeck
1Department of Cardiology, University of Antwerp, B-2610 Wilrijk, Belgium. emily@vanvre.be
Insights
Coronary artery disease (CAD) patients show reduced circulating myeloid and plasmacytoid dendritic cells (DCs), a systemic effect of atherosclerosis. These lower dendritic cell counts are not due to medication or endothelial dysfunction.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Atherosclerosis Research
Background:
- Previous research indicated a decline in circulating myeloid (m) and plasmacytoid (p) dendritic cells (DCs) in patients with coronary artery disease (CAD).
- This study aimed to further investigate total blood DC numbers and their relationship with CAD severity and endothelial function.
Purpose of the Study:
- To determine if the decline in circulating dendritic cells (DCs) in coronary artery disease (CAD) patients is associated with disease extent or type.
- To explore the relationship between DC numbers, endothelial function, and medication use in CAD patients.
Main Methods:
- Patients were categorized into control, stable one-vessel CAD, stable three-vessel CAD, and unstable one-vessel CAD groups.
- Total blood DCs, myeloid DCs (mDCs), and plasmacytoid DCs (pDCs) were quantified using specific markers (BDCA-1 for mDCs, BDCA-2 for pDCs).
- Endothelial function was assessed via flow-mediated dilatation (FMD) of the brachial artery.
Main Results:
- Numbers of total DCs, mDCs, and pDCs were significantly lower in CAD patients compared to controls, irrespective of CAD severity or type.
- Lower mDC counts were associated with increased interleukin-6 and high-sensitivity C-reactive protein.
- Increased mDCs were observed with impaired FMD and use of beta-blockers or lipid-lowering drugs, with additive effects noted.
Conclusions:
- The reduction in circulating DCs in CAD is a systemic effect of atherosclerosis, not directly caused by medication or endothelial dysfunction.
- Myeloid and plasmacytoid DCs appear to have distinct roles in inflammation during atherosclerosis, influenced differently by cytokines and treatments.
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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