Anti-allergic properties of antihistamines in humans

Citation
Rj. Davies et Jl. Devalia, Anti-allergic properties of antihistamines in humans, REV FR ALLE, 38(10), 1998, pp. 925-930
Citations number
22
Categorie Soggetti
Clinical Immunolgy & Infectious Disease
Journal title
REVUE FRANCAISE D ALLERGOLOGIE ET D IMMUNOLOGIE CLINIQUE
ISSN journal
03357457 → ACNP
Volume
38
Issue
10
Year of publication
1998
Pages
925 - 930
Database
ISI
SICI code
0335-7457(199812)38:10<925:APOAIH>2.0.ZU;2-Q
Abstract
The recent finding that an antihistamine administered regularly to 1-2 year s old children with atopic dermatitis, prevented the subsequent development of asthma in those allergic to grass pollen or house dust mite has focused attention on the properties of this class of therapeutic agents. Is this e ffect simply due to antagonism of histamine, which may have wider actions i n the development of airway inflammation than previously suspected, or is i t a result of the anti-allergic properties exhibited by the second generati on antihistamines! There are now many in vivo studies which have demonstrat ed that antihistamines decrease mast/basophil cell mediator release, inflam matory cell infiltration in allergic disease, and expression of adhesion mo lecules on epithelial cells. Numerous in vitro studies support these findin gs, extending the anti-inflammatory properties of antihistamines to decreas ing eosinophil migration and release of proinflammatory mediators. We have established primary cultures of epithelial cells from nasal biopsies from s easonal allergic rhinitics outside the pollen season, and studied the effec t of 0 to 10(-3)M fexofenadine, the main active metabolite of terfenadine, on activated eosinophil-induced changes in electrical resistance (a measure of permeability of epithelial cultures) and release of pro-inflammatory cy tokines and adhesion molecules. 10(-9) to 10(-3)M fexofenadine significantl y inhibited eosinophil-induced increases in the permeability of the epithel ial cell cultures and the release of IL-8, GM-CSF and sICAM-1. In addition, 10(-6) to 10(-3)M fexofenadine significantly inhibited cytokine-induced eo sinophil chemotaxis and adhesion of these cells to endothelial cells.