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Nitric oxide reduces T lymphocyte adhesion to human brain microvessel endothelial cells via a cGMP-dependent pathway.

Authors
  • Wong, Donald1
  • Prameya, Rukmini
  • Wu, Vivian
  • Dorovini-Zis, Katerina
  • Vincent, Steven R
  • 1 Department of Psychiatry and The Brain Research Centre, Section of Neuropathology, Vancouver Hospital, The University of British Columbia, Vancouver, B.C., Canada. , (Canada)
Type
Published Article
Journal
European Journal of Pharmacology
Publisher
Elsevier
Publication Date
May 09, 2005
Volume
514
Issue
2-3
Pages
91–98
Identifiers
PMID: 15910796
Source
Medline
License
Unknown

Abstract

The entry of lymphocytes into the brain is normally limited by the blood-brain barrier, however, during inflammation prominent lymphocytic infiltration occurs. In this study, we investigated the effects of nitric oxide (NO) on the adhesion of T cells to cultured human brain microvessel endothelial cells. T cell adhesion to unstimulated or tumor necrosis factor-alpha (TNF-alpha)-treated cells was quantified by counting the number of lymphocytes bound to the monolayer by light microscopy. TNF-alpha increased T cell adhesion in a time-dependent manner. Incubation of monolayers with NO donors decreased adhesion. This effect was blocked by a guanylyl cyclase inhibitor and mimicked by a cGMP agonist, and was thus dependent on the generation of cGMP. NO did not modulate adhesion molecule expression in the endothelial cells, suggesting an action on the T cells. Pre-treatment of T cells with NO or a cGMP agonist decreased binding to recombinant endothelial adhesion molecules. These findings suggest that NO can modulate the adhesion of T cells to human brain microvessel endothelial cells via a cGMP-dependent mechanism, and may thus regulate lymphocyte traffic during central nervous system inflammation.

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