F. Paolieri et al., Terfenadine and fexofenadine reduce in vitro ICAM-1 expression on human continuous cell lines, ANN ALLER A, 81(6), 1998, pp. 601-607
Background: Epithelial cells and fibroblasts play an important role in alle
rgic inflammation. Modulation of surface expression of adhesion molecules o
n epithelial cells by antiallergic drugs has been shown by both in vivo and
in vitro studies.
Objective: The aim of the study was to evaluate the effect exerted by terfe
nadine and fexofenadine on adhesion molecules expression (CD54/ICAM-1 and C
D29) of a human continuously cultured conjunctival epithelial cell line (WK
) and a fibroblast cell line (HEL).
Methods: By means of flow cytometry analysis, we evaluated ICAM-1 and CD29
expression by WK and HEL epithelial cells in basal condition (at baseline)
or after IFN gamma or TNF alpha stimulation in the presence or in the absen
ce of terfenadine and fexofenadine. We also performed immunoenzymatic assay
s in order to evaluate soluble ICAM-1 released by WK cells and procollagen
type I and III and IL6 released by HEL cells.
Results: Terfenadine and fexofenadine significantly reduced ICAM-1 basal ex
pression on WK cells at the concentration of 1 mu g/mL and 50 mu g/mL, resp
ectively. In addition, both terfenadine and fexofenadine were able to decre
ase soluble ICAM-1 levels in IFN gamma-stimulated WK cells. On HEL fibrobla
sts, fexofenadine only was able to inhibit ICAM-1 upregulation induced by I
FN gamma. Concerning the release of fibroblast products, we observed a dose
-dependent decrease of spontaneous IL6 release only in the presence of fexo
fenadine.
Conclusion: This study shows that terfenadine and fexofenadine exert a biol
ogic effect directly on epithelial cells and fibroblasts reducing ICAM-1 ex
pression and partially reducing soluble ICAM-1 release.