Cytokine-induced modulation of cellular adhesion to human cerebral endothelial cells is mediated by soluble vascular cell adhesion molecule-1

被引：84

作者：

Kallmann, BA ^{[1
]}

Hummel, V ^{[1
]}

Lindenlaub, T ^{[1
]}

Ruprecht, K ^{[1
]}

Toyka, KV ^{[1
]}

Rieckmann, P ^{[1
]}

机构：

[1] Univ Wurzburg, Clin Res Unit Multiple Sclerosis & Neuroimmunol, D-97080 Wurzburg, Germany

来源：

BRAIN | 2000年 / 123卷

关键词：

soluble adhesion molecules; multiple sclerosis; blood-brain barrier; VCAM-1; IFN-beta;

D O I：

10.1093/brain/123.4.687

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Tumour necrosis factor-alpha (TNF-alpha) 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-alpha 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-alpha-induced release of soluble VCAM-1 was further increased by cotreatment with interferon-beta (IFN-beta), while IFN-beta 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-alpha 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-beta treatment exerts protective effects in multiple sclerosis patients.

引用

页码：687 / 697

页数：11

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