Sicinska J, Gorska E, Cicha M, Kuklo-Kowalska A, Hamze V, Stepien K, Wasik M, Rudnicka L
Department of Dermatology, CSK MSWiA, Warsaw, Poland.
Clin Exp Rheumatol. 2008 Jul-Aug;26(4):527-33.
To evaluate serum levels of fractalkine (FKN), a mediator of leukocyte transmigration, C-reactive protein (CRP) and expression of integrins CD11a and CD49d on peripheral blood lymphocytes in systemic sclerosis (SSc) and to investigate whether they are modulated by intravenous prostaglandin E1 (PGE1).
Serum levels of fractalkine and C-reactive protein and expression of CD11a 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 microg-40 microg-60 microg) and after 4 weeks.
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<0.0001) and decreased significantly after PGE1 (5.16+/-1.27 ng/ml, p<0.05). After four weeks fractalkine level was still significantly lower than baseline 7.70+/-2.19 ng/ml (p<0.05). Basal percentage of CD11a (+) nor CD49d (+) lymphocytes in SSc (82.38+/-1.60%, 70.74+/-1.68%, respectively) did not differ from controls (85.73+/-2.04%, 75.62+/-2.48%; respectively, p>0.05). PGE1 treatment resulted in decrease of both CD11a (+) (67.72+/-3.34%, p<0.0001) and CD49d (+) lymphocytes (65.32+/-1.62%, p<0.0001). After 4 weeks the percentage of CD11a (+) 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+/-2.01 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+/-2.19 ng/ml) was significantly lower than baseline (p<0.05).
Fractalkine may play an important role in the pathogenesis of vascular dysfunction in systemic sclerosis. Prostaglandin E1 down-regulates serum fractalkine level, as well as CD11a and CD49d expression on peripheral blood lymphocytes, which suggests additional mechanisms in which this vasodilatatory agent exerts its efficacy in systemic sclerosis.
评估趋化因子（FKN，一种白细胞迁移介质）、C反应蛋白（CRP）的血清水平以及系统性硬化症（SSc）患者外周血淋巴细胞上整合素CD11a和CD49d的表达，并研究它们是否受静脉注射前列腺素E1（PGE1）的调节。
对50例SSc患者和18名健康对照者评估趋化因子和C反应蛋白的血清水平以及外周血淋巴细胞上CD11a和CD49d的表达。在25例SSc患者中，连续3天每日输注PGE1（20μg - 40μg - 60μg）后及4周后，对研究参数再次进行评估。
在SSc患者中，趋化因子基础水平显著高于对照组（9.04±1.79 ng/ml对1.17±0.1 ng/ml；p<0.0001），PGE1治疗后显著降低（5.16±1.27 ng/ml，p<0.05）。4周后，趋化因子水平仍显著低于基线水平7.70±2.19 ng/ml（p<0.05）。SSc患者中CD11a(+)和CD49d(+)淋巴细胞的基础百分比（分别为82.38±1.60%、70.74±1.68%）与对照组（分别为85.73±2.04%、75.62±2.48%；p>0.05）无差异。PGE1治疗导致CD11a(+)淋巴细胞（67.72±3.34%，p<0.0001）和CD49d(+)淋巴细胞（65.32±1.62%，p<0.0001）均减少。4周后，CD11a(+)和CD49d(+)淋巴细胞百分比仍显著低于基线水平（分别为77.80±2.47%和65.32±1.62%，均p<0.001）。在SSc患者中，CRP基础水平显著高于对照组（4.70±2.01 mg/dl对1.40±1.79 mg/dl，p<0.005），PGE1治疗后显著降低（3.39±2.06 mg/dl，p<0.05）。4周后，CRP水平（4.38±2.19 ng/ml）显著低于基线水平（p<0.05）。
趋化因子可能在系统性硬化症血管功能障碍的发病机制中起重要作用。前列腺素E1可下调血清趋化因子水平以及外周血淋巴细胞上CD11a和CD49d的表达，这提示这种血管扩张剂在系统性硬化症中发挥作用的其他机制。
