Degranulation of eosinophils mediated by intercellular adhesion molecule-1and its ligands is involved in adhesion molecule expression on endothelialcells-selective induction of VCAM-1

Citation
J. Chihara et al., Degranulation of eosinophils mediated by intercellular adhesion molecule-1and its ligands is involved in adhesion molecule expression on endothelialcells-selective induction of VCAM-1, J ALLERG CL, 103(5), 1999, pp. S452-S456
Citations number
38
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
ISSN journal
00916749 → ACNP
Volume
103
Issue
5
Year of publication
1999
Part
2
Supplement
S
Pages
S452 - S456
Database
ISI
SICI code
0091-6749(199905)103:5<S452:DOEMBI>2.0.ZU;2-6
Abstract
Background: Adhesion molecules and eosinophils may play an important role i n the pathogenesis of allergic inflammatory reactions. Objective: We attempted to clarify eosinophil activation, such as degranula tion, by signaling through adhesion molecule and to determine whether degra nulation is involved in adhesion molecule expression on endothelial cells. Methods: Eosinophils were cultured with or without recombinant soluble inte rcellular adhesion molecule-1 (ICAM-1), and the levels of eosinophil cation ic protein and eosinophil-derived neurotoxin were determined. The influence of these eosinophil granule proteins or supernatant from eosinophil cultur ed with ICAM-1 on the expression of ICAM-1 or vascular cell adhesion molecu le-1 (VCAM-1) on endothelial cells was also examined by flow-cytometric ana lysis. Results: Supernatant levels of eosinophil granule protein mere significantl y increased by culture for 4 hourss or 16 hours with recombinant soluble IC AM-1, suggesting degranulation by adherence to ICAM-1. Both granule protein s and the supernatants of eosinophils cultured with recombinant soluble ICA M-1 induced expression of ICAM-1 and VCAM-1 on endothelial cells, with the latter showing a more prominant increase. Conclusion: Degranulation mediated through adherence to endothelial cells b y ICAM-1 and its ligands may be involved in the expression of adhesion mole cules, such as ICAM-1 or VCAM-1, on these cells. Our finding of the selecti ve induction of VCAM-1 expression suggests that eosinophil adherence to end othelial cells, even if it is because of ICAM-1, may be involved in selecti ve eosinophil recruitment and accumulation at sites of allergic inflammatio n.