Endothelial dysfunction is independent of inflammation and altered CCR7 T cell expression in patients with ankylosing spondylitis

Objective The accumulation of CCR7 (chemokine receptor 7) positive cells in the vessel wall may be involved in endothelial dysfunction and subsequent accelerated atherogenesis. CCR7 plays a crucial role in T cell and monocyte migration / homing and in priming of naive T lymphocytes in non-lymphoid tissues in chronic inflammatory diseases. Our objective was to investigate the endothelial function and inflammation-driven expression of CCR7 on T lymphocytes in patients with ankylosing spondylitis (AS). Methods We performed flow cytometry to assess the distribution of peripheral blood T cell subpopulations in the context of serum inflammatory markers (TNF-alpha, IL-6, sICAM-1) and asymmetric dimethylarginine (ADMA) in 38 patients with AS with active disease, and in 20 healthy controls. Results Patients with AS demonstrated higher ADMA (0.74 +/- 0.2 mu mol/l vs. 0.64 +/- 0.15 mu mol/l; p=0.03), as well as elevated inflammatory markers (TNF alpha, IL-6, sICAM-1) and increased proportions of circulating CCR7-positive lymphocytes largely attributable to elevated CD8(+) naive T cells (47.1 +/- 17 vs. 34.3 +/- 13.1%; p=0.005). However, ADMA did not correlate with either CCR7-positive lymphocytes or inflammatory markers. Conclusion We found an increased percentage of peripheral CCR7 T cells accompanied by endothelial dysfunction in patients with AS. The lack of direct associations between ADMA and inflammation may suggest the presence of other pathogenic mechanisms contributing to accelerated atherogenesis and increased cardiovascular risk in AS.