Dekkers P E, ten Hove T, te Velde A A, van Deventer S J, van Der Poll T
Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Infect Immun. 2000 Apr;68(4):2156-60. doi: 10.1128/IAI.68.4.2156-2160.2000.
The receptor for urokinase-type plasminogen activator (uPAR) (CD87) plays an important role in leukocyte adhesion and migration. To assess the effect of endotoxin on cellular uPAR, uPAR expression was determined on leukocytes by fluorescence-activated cell sorter analysis in seven healthy subjects following intravenous injection of endotoxin (lot G; 4 ng/kg). Endotoxin induced a transient increase in uPAR expression on monocytes, reaching a 92% +/- 46% increase over baseline expression after 6 h (P < 0.05). Endotoxin did not influence uPAR expression on granulocytes, while uPAR remained undetectable on lymphocytes. Endotoxin also increased soluble uPAR levels in plasma (P < 0.05). Stimulation of human whole blood with endotoxin or gram-positive stimuli in vitro also resulted in an upregulation of monocyte uPAR expression. Although tumor necrosis factor alpha (TNF) upregulated monocyte uPAR expression, anti-TNF did not influence the endotoxin-induced increase in monocyte uPAR expression. These data suggest that infectious stimuli may influence monocyte function in vivo by enhancing the expression of uPAR.
尿激酶型纤溶酶原激活物(uPAR)受体(CD87)在白细胞黏附和迁移中起重要作用。为评估内毒素对细胞uPAR的影响,对7名健康受试者静脉注射内毒素(批号G;4 ng/kg)后,通过荧光激活细胞分选分析测定白细胞上的uPAR表达。内毒素诱导单核细胞上uPAR表达短暂增加,6小时后比基线表达增加92%±46%(P<0.05)。内毒素不影响粒细胞上的uPAR表达,而淋巴细胞上未检测到uPAR。内毒素还增加了血浆中可溶性uPAR水平(P<0.05)。体外使用内毒素或革兰氏阳性刺激物刺激人全血也导致单核细胞uPAR表达上调。虽然肿瘤坏死因子α(TNF)上调了单核细胞uPAR表达,但抗TNF并不影响内毒素诱导的单核细胞uPAR表达增加。这些数据表明,感染性刺激可能通过增强uPAR表达在体内影响单核细胞功能。