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Endothelial cells modulate eosinophil surface markers and mediator release

Unité de Recherche en Pneumologie, Centre de Recherche de l'Hôpital Laval, Institut Universitaire de Cardiologie et de Pneumologie de l'Université Laval, Quebec, Canada

CORRESPONDENCE: M. Laviolette, Hôpital Laval, 2725 Chemin Sainte-Foy, Québec, PQ, G1V 4G5, Canada. Fax: 1 4186564762. E-mail: Michel.Laviolette@med.ulaval.ca

Keywords: CD35, CD69, human umbilical vein endothelial cells, leukotriene C4, transmigration

Received: November 7, 2002
Accepted January 21, 2003

This study was supported by the Canadian Institutes of Health Research, Ottawa, Canada (MOP-49534).

Migration from blood to tissue modulates eosinophil function, possibly through interactions with endothelial cells.

The effects of contact with and migration through endothelial cells on eosinophil expression of surface markers and release of leukotriene C₄ were evaluated.

A small proportion (2.6%) of eosinophils spontaneously migrated through endothelial cell monolayers. Activation of endothelial cells by interleukin (IL)-4 or IL-1ß slightly increased this migration (to 12.4%), which became much greater when a chemoattractant was placed in the lower chamber (84.3%). However, the chemotactic effect was downregulated by pretreating endothelial cells with interferon gamma (IFN-; 63.1%). At baseline, 5% of eosinophils expressed CD69; this increased to 30.7% in culture on untreated endothelial cells and to 50.9% on IL-1ß-pretreated endothelial cells. This effect was mediated through intercellular adhesion molecule-1/CD11b interaction. Eosinophil migration through endothelial cells further increased CD69 expression to 63.9% and also increased CD35 expression from 83.3 to 91.3%. Upon stimulation, eosinophils that had migrated through endothelial cells produced more leukotriene C₄ than control cells (872.4 and 103.9 pg·mL^–1, respectively). Endothelial cell pretreatment with IL-4 or IL-1ß further increased leukotriene C₄ release (1,789.1 and 2,895.1 pg·mL^–1, respectively), whereas pretreatment with IFN- decreased it (293.7 pg·mL^–1).

These data show that in vitro interactions with endothelial cells upregulate eosinophil membrane receptor expression and mediator release and that these effects are differently modulated by T-helper cell type 1 and 2 cytokines. These eosinophil modulations may play an important role in asthma pathogenesis.

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