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Published on: October 17, 2017
Blood monocyte heterogeneity and markers of endothelial activation in ankylosing spondylitis
Andrzej Surdacki1, Joanna Sulicka, Mariusz Korkosz
1From the Second Department of Cardiology, the Department of Rheumatology and Balneology, the Division of Rheumatology, Department of Internal Medicine and Gerontology, and the Department of Internal and Agricultural Medicine, Jagiellonian University Medical College and University Hospital; and J. Dietl Hospital, Krakow, Poland.
Insights
Ankylosing spondylitis patients show altered monocyte subsets and increased endothelial activation, suggesting immune dysregulation contributes to cardiovascular risk. These changes are more pronounced in active disease, potentially accelerating atherosclerosis.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Rheumatology
Background:
- Ankylosing spondylitis (AS) is linked to increased cardiovascular (CV) morbidity.
- Activated endothelium and monocyte interactions are early steps in atherosclerosis.
- Understanding these interactions in AS is crucial for CV risk assessment.
Purpose of the Study:
- To quantify blood monocyte subsets in AS patients.
- To assess monocyte subsets in relation to endothelial activation.
- To evaluate immune dysregulation in AS patients without clinical CV disease.
Main Methods:
- Studied 47 AS patients and 22 controls, excluding those with CV disease or risk factors.
- Used flow cytometry to identify classical, intermediate, and nonclassical monocyte subsets.
- Measured markers of inflammation and endothelial activation, including soluble intercellular adhesion molecule-1 and monocyte CD11b expression.
Main Results:
- AS patients had higher classical and lower nonclassical monocyte counts compared to controls.
- Elevated soluble intercellular adhesion molecule-1 was observed in AS patients.
- Increased CD11b expression on monocytes correlated with disease activity (Bath Ankylosing Spondylitis Disease Activity Index ≥ 4) and IL-6 levels.
Conclusions:
- Immune dysregulation contributes to heightened monocyte-endothelial interactions in AS.
- These interactions may accelerate atherogenesis over time, particularly in patients with active disease.
- Findings highlight a potential mechanism for increased CV risk in ankylosing spondylitis.
Objective:
Ankylosing spondylitis (AS) is associated with excessive cardiovascular (CV) morbidity. Interactions between activated endothelium and monocytes precede atherosclerotic plaques. Our aim was to quantify blood monocyte subsets in relation to endothelial activation and inflammatory activity in subjects with AS who were free of clinical atherosclerotic CV disease.
Methods:
Markers of inflammation and endothelial activation were measured in 47 patients with AS receiving no disease-modifying antirheumatic drugs, and 22 healthy controls. Exclusion criteria included atherosclerotic CV disease and traditional risk factors. Flow cytometry was used to identify monocyte subsets: classical CD14(++)CD16(-), intermediate CD14(++)CD16(+), and nonclassical CD14(+)CD16(++) monocytes and to evaluate their expression of CD11b and CD11c.
Results:
Traditional risk factors were comparable among the groups, except for lower high-density lipoprotein cholesterol in AS (p = 0.007). Relative to controls, in subjects with AS counts of classical monocytes were higher (84.3 ± 5.4 vs 78.9 ± 5.3% of blood monocytes, p < 0.001) and nonclassical monocytes lower (2.9 ± 2.2 vs 5.5 ± 2.3%, p < 0.001). In AS we observed increased soluble intercellular adhesion molecule-1 [251 (224-293) vs 202 (187-230) ng/ml, p = 0.002], an endothelial ligand for monocytic β2-integrin CD11b/CD18. CD11b expression on all 3 monocyte subsets was elevated in 21 AS subjects with a Bath Ankylosing Spondylitis Disease Activity Index score ≥ 4 versus the remaining patients (p = 0.005-0.03). C-reactive protein, interleukin 6 (IL-6), and pentraxin-3 were increased in AS, in contrast to tumor necrosis factor-α and IL-18. IL-6 correlated with classical monocytes numbers in AS (r = 0.56, p < 0.0001) but not in the controls (r = 0.10, p = 0.65).
Conclusion:
Our findings suggest a contribution of immune dysregulation to enhanced monocyte-endothelial interactions in AS, especially in patients with active disease, which possibly can accelerate atherogenesis on a longterm basis.
