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The Journal of Immunology, Vol 157, Issue 3 1233-1241, Copyright © 1996 by American Association of Immunologists
ARTICLES |
Y Rival, A Del Maschio, MJ Rabiet, E Dejana and A Duperray
Atomic Energy Commission, Laboratory of Hematology, INSERM Unit 217, Department of Molecular and Structural Biology, Center for Nuclear Studies (CEN), Grenoble, France.
Endothelial cell (EC) junctions regulate circulating leukocyte extravasation and infiltration at inflammatory sites. Several lines of evidence show that platelet endothelial cell adhesion molecule-1 (PECAM- 1), a specific component of EC junctions, is required for leukocyte transmigration through EC monolayers. In this paper, we examined the effects of two inflammatory cytokines, TNF-alpha and IFN-gamma, on PECAM-1 and vascular endothelial-cadherin/catenin organization. We found that the addition of inflammatory cytokines (TNF-alpha plus IFN- gamma in combination, for > or = 24 h) caused PECAM-1 to disappear from EC intercellular contacts. Confocal microscopy indicated that after treatment with the cytokines, PECAM-1 was rapidly internalized. In addition, a strong inhibition of PECAM-1 synthesis and a decrease in PECAM-1 mRNA were observed. This phenomenon was only found when TNF- alpha plus IFN-gamma were used in combination. Adhesion of polymorphonuclear cells to doubly treated EC was increased compared with control cells or cells incubated with TNF-alpha or IFN-gamma separately. This was correlated with an increased expression of intercellular adhesion molecule-1. However, the disappearance of PECAM- 1 from cell junctions after treatment with TNF-alpha plus IFN-gamma was accompanied by a marked reduction of leukocyte migration through EC monolayers. The correlation between PECAM-1 level and leukocyte transmigration was supported by transmigration inhibition assays using blocking anti-PECAM-1 mAb. These data indicate that PECAM-1 is a specific target of inflammatory cytokines and suggest that changes in its synthesis and organization might negatively modulate leukocyte recruitment.
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