Upregulation of intercellular adhesion molecule-1 expression on human endothelial cells by tumour necrosis factor-α in an in vitro model of the blood–brain barrier

• Published in: Brain research 1999-06, Vol.830 (2), p.330-336
• Main Authors: Dobbie, Michael S., Hurst, Roger D., Klein, Nigel J., Surtees, Robert A.H.
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood-Brain Barrier - drug effects; Blood–brain barrier; CD36; CD36 Antigens - analysis; Cell Line; Cerebral circulation. Blood-brain barrier. Choroid plexus. Cerebrospinal fluid. Circumventricular organ. Meninges; Cerebral malaria; E-selectin; E-Selectin - metabolism; Endothelial cell; Endothelium, Vascular - cytology; Endothelium, Vascular - drug effects; Endothelium, Vascular - metabolism; Flow Cytometry; Fundamental and applied biological sciences. Psychology; Humans; Intercellular adhesion molecule-1; Intercellular Adhesion Molecule-1 - metabolism; Rats; Tumor Cells, Cultured; Tumor Necrosis Factor-alpha - pharmacology; Up-Regulation; Vascular cell adhesion molecule-1; Vascular Cell Adhesion Molecule-1 - metabolism; Vertebrates: nervous system and sense organs
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(99)01436-5

Adhesion molecules on the endothelial surface of the blood–brain barrier (BBB) play an important role in the pathogenesis of many encephalopathies, including multiple sclerosis (MS) and cerebral malaria (CM). The expression of four surface molecules of relevance to MS and CM on the immortalized human umbilical vein endothelial cell line, ECV304, was investigated using immunofluorescence flow cytometry. We found that ECV304 cells express intercellular adhesion molecule-1 (ICAM-1) and low levels of CD36, but not vascular cell adhesion molecule-1 (VCAM-1) or E-selectin. This expression pattern was unaltered on ECV304 cells which were co-cultured with C6 glioma cells; conditions under which the endothelial cells display enhanced barrier formation. Tumour necrosis factor-α (TNF-α), which is elevated in MS and CM, decreased the integrity of the barrier in co-cultured endothelial cells and upregulated the expression of ICAM-1 nine-fold. The significance of elevated ICAM-1 expression in relation to the binding of parasitised erythrocytes at the BBB in CM is discussed.