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

Eur J Pharmacol. 2005 May 9;514(2-3):91-8. doi: 10.1016/j.ejphar.2005.03.025.

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.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Brain / blood supply
  • Cell Adhesion / drug effects
  • Cell Adhesion / physiology
  • Cells, Cultured
  • Cyclic GMP / analogs & derivatives*
  • Cyclic GMP / metabolism*
  • Cyclic GMP / pharmacology
  • Dose-Response Relationship, Drug
  • E-Selectin / pharmacology
  • Endothelial Cells / cytology*
  • Enzyme Inhibitors / pharmacology
  • Guanylate Cyclase / antagonists & inhibitors
  • Humans
  • Intercellular Adhesion Molecule-1 / pharmacology
  • NG-Nitroarginine Methyl Ester / pharmacology
  • Nitric Oxide / physiology*
  • Nitric Oxide Donors / pharmacology
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Nitroprusside / pharmacology
  • Nitroso Compounds / pharmacology
  • Oxadiazoles / pharmacology
  • Platelet Endothelial Cell Adhesion Molecule-1 / pharmacology
  • Quinoxalines / pharmacology
  • Signal Transduction / physiology*
  • T-Lymphocytes / cytology*
  • Tumor Necrosis Factor-alpha / pharmacology
  • Vascular Cell Adhesion Molecule-1 / pharmacology

Substances

  • 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one
  • E-Selectin
  • Enzyme Inhibitors
  • Nitric Oxide Donors
  • Nitroso Compounds
  • Oxadiazoles
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Quinoxalines
  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • 2,2'-(hydroxynitrosohydrazono)bis-ethanamine
  • Nitroprusside
  • 8-bromocyclic GMP
  • Nitric Oxide
  • Nitric Oxide Synthase
  • Guanylate Cyclase
  • Cyclic GMP
  • NG-Nitroarginine Methyl Ester