Brain, Vol. 123, No. 4, 687-697,
April 2000
© 2000 Oxford University Press
Cytokine-induced modulation of cellular adhesion to human cerebral endothelial cells is mediated by soluble vascular cell adhesion molecule-1
Clinical Research Unit for Multiple Sclerosis and Neuroimmunology, University of Würzburg, Germany
Correspondence to:
Dr Boris A. Kallmann, Clinical Research Unit for Multiple Sclerosis and Neuroimmunology, Julius-Maximilians-Universität, Josef-Schneider-Strasse 11, D 97080 Würzburg, Germany E-mail: b.kallmann{at}mail.uni-wuerzburg.de
Tumour necrosis factor-
( TNF-) has been proposed as one of the key mediators of inflammatory diseases of the CNS such as multiple sclerosis. It has been shown to induce the expression of adhesion molecules which is a prerequisite for the transmigration of immune cells through the blood–brain barrier. We therefore investigated the role of TNF- in the expression and release of vascular cell adhesion molecule-1 (VCAM-1) in cultures of human cerebral endothelial cells (HCEC) in comparison with peripheral blood mononuclear cells (PBMC). A time- and dose-dependent expression of VCAM-1 and release of soluble VCAM-1 was detected in HCEC but not PBMC. TNF--induced release of soluble VCAM-1 was further increased by cotreatment with interferon-ß (IFN-ß), while IFN-ß alone did not affect VCAM-1 expression or the release of soluble VCAM-1. In addition, we observed that preincubation of PBMC with soluble VCAM-1 completely blocked their adhesion to HCEC. In conclusion, the proinflammatory effect of TNF- on HCEC, which involves the induction of VCAM-1 expression and cellular adhesion, is followed by the consecutive effects of soluble VCAM-1 release in blocking adhesion and downregulating further cellular infiltration. Increasing soluble VCAM-1 release during active inflammation could be another mechanism by which IFN-ß treatment exerts protective effects in multiple sclerosis patients.
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