Regulation of ICAM-(3) and other adhesion molecule expressions on eosinophils in vitro. Effects of dexamethasone

Citation
M. Juan et al., Regulation of ICAM-(3) and other adhesion molecule expressions on eosinophils in vitro. Effects of dexamethasone, ALLERGY, 54(12), 1999, pp. 1293-1298
Citations number
22
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
ALLERGY
ISSN journal
01054538 → ACNP
Volume
54
Issue
12
Year of publication
1999
Pages
1293 - 1298
Database
ISI
SICI code
0105-4538(199912)54:12<1293:ROIAOA>2.0.ZU;2-B
Abstract
Background: ICAM-3 has been recently identified as the third leukocyte-func tion associated-1 (LFA-1) ligand. ICAM-3 is expressed in eosinophils, but i ts regulation has not been studied. The objective of this study was to inve stigate the differential expression of ICAM-3 and other adhesion molecules (AM) on the surface of eosinophils. We also evaluated the effects of dexame thasone on AM expression. Methods: Normodense eosinophils were isolated from peripheral blood and inc ubated with calcium ionophore A23187 (calcimycin) with and without dexameth asone. Expression of AM was assessed by flow cytometry and expressed as flu orescence mean intensity (FMI). Results: Peripheral blood eosinophils constitutively expressed low levels o f ICAM-1 and ICAM-2 (<10 FMI), moderate levels (10-50 FMI) of CD29 and L-se lectin, and high levels (>50 FMI) of ICAM-3, LFA-1, and Mac-1. Calcium iono phore (1 mu M) significantly increased Mac-1 and ICAM-1 expression at 6 and 24 h. L-selectin expression decreased at 6 and 24 h, but ICAM-2, ICAM-3, L FA-I, and CD29 expression did not show any significant change after calcium ionophore stimulation. Dexamethasone decreased ICAM-3 and increased L-sele ctin basal expression, and it caused a dose-related inhibition of calcium i onophore-induced ICAM-1 expression. Conclusions: These findings suggest that some AM, such as ICAM-1, Mac-1, an d L-selectin, may be involved in adhesion during eosinophil activation and that glucocorticoids may prevent airway inflammation by regulating the expr ession of AM in eosinophils. The role of ICAM-3, a leukocyte AM highly expr essed in resting eosinophils, remains to be clarified.