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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Heterogeneity of peripheral blood monocytes, endothelial dysfunction and subclinical atherosclerosis in patients with
T P Mikołajczyk1, G Osmenda1, B Batko2
1Translational Medicine Laboratory, Department of Internal Medicine, Jagiellonian University School of Medicine, Krakow, Poland.
Insights
Systemic lupus erythematosus (SLE) patients show increased subclinical atherosclerosis linked to specific proinflammatory monocytes (CD14dimCD16+). This association with atherosclerosis appears independent of endothelial dysfunction in SLE patients.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Rheumatology
Background:
- Systemic lupus erythematosus (SLE) is linked to higher cardiovascular risks.
- Mechanisms behind increased subclinical atherosclerosis in SLE patients are not fully understood.
- Monocytes play a role in atherosclerosis, prompting investigation in SLE.
Purpose of the Study:
- To explore the connection between subclinical atherosclerosis, endothelial dysfunction, and monocyte phenotypes in SLE patients.
- To identify specific monocyte subsets associated with atherosclerosis in SLE.
Main Methods:
- Monocyte subsets (CD14, CD16) were analyzed in 42 SLE patients and 42 controls.
- Carotid intima-media thickness (IMT) and brachial artery flow-mediated dilation (FMD) were measured via ultrasonography.
- Nitroglycerin-induced dilation (NMD) was also assessed.
Main Results:
- SLE patients exhibited modestly increased IMT compared to controls.
- Significant endothelial dysfunction was observed in SLE patients.
- A positive correlation was found between CD14dimCD16+ proinflammatory monocytes and IMT in SLE patients, but not in controls.
- Endothelial dysfunction (FMD) did not correlate with any monocyte subsets.
Conclusions:
- CD14dimCD16+ monocytes are associated with subclinical atherosclerosis in SLE patients.
- The mechanism linking these monocytes to atherosclerosis in SLE appears independent of endothelial dysfunction.
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.
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