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

Boris Kallmann | Zendy

Open Access

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

Author(s) -

Boris Kallmann

Publication year - 2000

Publication title -

brain

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.142

H-Index - 336

eISSN - 1460-2156

pISSN - 0006-8950

DOI - 10.1093/brain/123.4.687

Subject(s) - vcam 1 , cell adhesion molecule , cell adhesion , tumor necrosis factor alpha , peripheral blood mononuclear cell , soluble cell adhesion molecules , cytokine , proinflammatory cytokine , neural cell adhesion molecule , microbiology and biotechnology , immunology , inflammation , intercellular adhesion molecule 1 , chemistry , icam 1 , biology , cell , in vitro , biochemistry

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.

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