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. 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
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.