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Published on: February 28, 2013
Dendritic cell activation is blunted in patients with coronary artery disease and diabetes mellitus
Gulay Imadoglu Yetkin1, Aysegul Atak Yucel2, İshak Özel Tekin3
1IMC Hospital International Medical Center Division of Microbiology, Mersin, Turkey.
Insights
Dendritic cell (DC) activation by oxidized LDL is blunted in patients with coronary artery disease (CAD), especially those with diabetes mellitus (DM). This suggests impaired immune responses in CAD patients with diabetes.
Area of Science:
- Immunology
- Cardiology
- Metabolic Diseases
Background:
- Dendritic cells (DCs) are crucial immune cells.
- Diabetic patients with unstable angina pectoris (UAP) show more mature and activated DCs.
- Previous findings suggest altered DC function in diabetic cardiovascular disease.
Purpose of the Study:
- To assess dendritic cell (DC) activation in patients with coronary artery disease (CAD) with and without diabetes mellitus (DM).
- To compare DC activation in these groups to subjects with normal coronary arteries (NCA).
Main Methods:
- Peripheral blood DCs from 23 severe CAD patients and 6 NCA subjects were analyzed.
- DC activation was measured using flow cytometry for CD86 expression.
- Cells were stimulated with oxidized low-density lipoprotein (ox-LDL).
Main Results:
- DC activation by ox-LDL was significantly increased in CAD patients without DM compared to controls.
- However, DC activation was not significantly increased in CAD patients with DM.
- NCA subjects without DM showed marked CD86 activation after ox-LDL stimulation.
Conclusions:
- DC activation upon ox-LDL stimulation is blunted in CAD patients compared to NCA subjects.
- This defective DC activation is more pronounced in diabetic patients with CAD.
- Impaired DC function may contribute to the pathophysiology of CAD in diabetic individuals.
Background:
It has been shown that functional status of dendritic cells (DCs) in diabetic patients with unstable angina pectoris (UAP) are more mature and activated than diabetic patients without coronary artery disease (CAD) and none diabetic patients with UAP. Accordingly we aimed to assess the activation of DCs in patients with CAD with/and without Diabetes Mellitus (DM) and compare to those in subjects with normal coronary arteries (NCA).
Materials And Methods:
Twenty three patients with severe CAD who were scheduled to coronary artery by-pass grafting surgery and 6 patients with angiographycally NCAs were included in the study. Activation of peripheral blood DCs have been analyzed by flow cytometric measures of CD86 activation.
Results:
In patients with CAD and without DM, DC activation significantly increased after stimulation of oxidesized LDL (135 ± 121 vs 248 ± 197 p = 0.024). However this activation didn't significantly increased in patients with CAD and DM (100 ± 20 vs 120 ± 97, p = 0,54). Patients with NCAs and without DM showed marked activation of CD86 after stimulation with ox-LDL.
Conclusion:
We have documented that DC activation, upon stimulation of ox-LDL has blunted in patients with CAD compared to patients with NCAs. Moreover this defective activation is more pronounced in those with diabetic patients with CAD.
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