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Am J Physiol Lung Cell Mol Physiol 277: L802-L810, 1999;
1040-0605/99 $5.00
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Vol. 277, Issue 4, L802-L810, October 1999

Augmentation of eosinophil degranulation and LTC4 secretion by integrin-mediated endothelial cell adhesion

Nilda M. Muñoz1, Kimm J. Hamann1, Klaus F. Rabe2, Hiroyuki Sano1, Xiangdong Zhu1, and Alan R. Leff1,3

1 Section of Pulmonary and Critical Care Medicine, Department of Medicine, and 3 Committees on Clinical Pharmacology and Cell Physiology, Division of the Biological Sciences, The University of Chicago, Chicago, Illinois 60637; and 2 Krankenhaus Grosshansdorf, LVA Hamburg D-22927, Grosshansdorf, Germany

We examined the effect of eosinophil ligation to cultured human umbilical vein endothelial cells (HUVECs) in augmenting the stimulated secretion of leukotriene (LT) C4 and eosinophil peroxidase (EPO). The effects of adhesion were compared before and after specific blockade with monoclonal antibodies directed against eosinophil surface integrins or endothelial counterligands. Adhesion to HUVECs augmented EPO release caused by formyl-methionyl-leucyl-phenylalanine plus cytochalasin B from 403 ± 15.3 (BSA control) to 778 ± 225 ng/106 cells for eosinophils exposed to interleukin-1alpha -treated HUVECs (P < 0.05) and also caused a twofold increase in stimulated LTC4 secretion (P < 0.05). To determine whether augmented secretion resulted directly from adhesive ligation, studies were also performed with paraformaldehyde-treated HUVECs; stimulated secretion of LTC4 from eosinophils was comparable to that for living HUVECs. Our study is the first demonstration that adhesion to HUVECs through ligation to alpha 4- or beta 2-integrin on the eosinophil surface causes augmentation of stimulated secretion of both EPO and LTC4 and that blockade of adhesion molecules on either eosinophils or HUVECs prevents the priming effect on eosinophil secretion.

eosinophils; adhesion molecules; leukotriene C4; eosinophil peroxidase


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