Increased serum fractalkine in systemic sclerosis. Down-regulation by prostaglandin E1.

Objectives To evaluate serum levels of fractalkine (FKN), a mediator of leukocyte transmigration, C-reactive protein (CRP) and expression of integrins CDlla and CD49d on peripheral blood lymphocytes in systemic sclerosis (SSc) and to investigate whether they are modulated by intravenous prostaglandin El (PGE1). Methods Serum levels of fractalkine and C-reactive protein and expression of CDlla and CD49d on peripheral blood lymphocytes were assessed in 50 SSc patients and in 18 healthy controls. In 25 SSc patients studied parameters were evaluated also after 3 consecutive daily PGE1 infusions (20 μg-40 μg-60 μg) and after 4 weeks. Results In SSc fractalkine basal level was significantly higher than in controls (9.04±1.79 ng/ml vs. 1.17±0.1 ng/ml; p 0.05). PGE1 treatment resulted in decrease of both CDlla (+) (67.72±3.34%, p<0.0001) and CD49d (+) lymphocytes (65.32±1.62%, p<0.0001). After 4 weeks the percentage of CDlla (+) and CD49d (+) lymphocytes remained significantly lower than at baseline (77.80±2.47% and 65.32±1.62%, respectively, both p<0.001). In SSc CRP basal level was significantly higher than in controls (4.70±2.0l mg/dl vs. 1.40±1.79 mg/dl, p<0.005) and reduced significantly after PGE1 (3.39±2.06 mg/dl, p<0.05). After 4 weeks, CRP level (4.38±2.l9 ng/ml) was significantly lower than baseline (p<0.05). Conclusion Fractalkine may play an important role in the pathogenesis of vascular dysfunction in systemic sclerosis. Prostaglandin El down-regulates serum fractalkine level, as well as CDlla and CD49d expression on peripheral blood lymphocytes, which suggests additional mechanisms in which this vasodilatatory agent exerts its efficacy in systemic sclerosis.