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Interleukin-4 counteracts pyrogen-induced downregulation of thrombomodulin
in cultured human vascular endothelial cells
S Kapiotis, J Besemer, D Bevec, P Valent, P Bettelheim, K Lechner and W Speiser
First Medical Department, University of Vienna, Austria.
Inflammatory mediators such as tumor necrosis factor (TNF) or interleukin-1
(IL-1) and bacterial lipopolysaccharides (LPS) were shown to shift the
hemostatic balance of the endothelial cell (EC) surface in favor of
procoagulant activities by inducing tissue factor (TF) expression and
downregulation of thrombomodulin (TM). In the present study, the effects of
IL-4 on these regulatory mechanisms were investigated using cultured human
umbilical vein EC. TM downregulation induced by the pyrogens IL-1 (100
U/mL), TNF (500 U/mL), and LPS (20 micrograms/mL) to less than 50% of TM
activity of untreated cells during a 12-hour incubation period was
completely neutralized when these mediators were coincubated with IL-4 (100
U/mL). In accordance with TM surface activity, TM messenger RNA was
decreased by IL-1, TNF, and LPS to less than 40% of untreated cells; this
effect was in part antagonized by IL-4. No influence of IL-4 on EC tissue
factor induction by IL-1, TNF, and LPS was found. Binding studies using
125I- radiolabeled IL-4 suggest that EC express a single class of high-
affinity binding sites (kd = 3.2 pmol/L; 2,000 to 2,500 receptors per
cell). These results show that IL-4, in part, protects the EC surface
against pyrogen-induced procoagulant changes. Transcriptional regulatory
mechanisms seem to be involved in EC surface TM regulation.
Volume 78,
Issue 2,
pp. 410-415,
07/15/1991
Copyright © 1991 by The American Society of Hematology
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