Levocetirizine (LCTR) possesses a variety of anti-inflammatory properties explaining the high efficacy in a variety of allergic disorders. In allergic rhinitis, the clinical response to LCTR includes an effective activity of all symptoms, including reversal of nasal obstruction. This observation rises the possibility that LCTR could act also on cells involved in airway remodelling such as fibroblasts. With this background, the aim of the study was to evaluate the ability of LCTR to downregulate fibroblast functions related to nasal inflammation and remodelling, i.e. adhesion molecule expression. Primary nasal polyp tissue-derived fibroblasts were stimulated with cytokines (TNF-α+IL4) or histamine (H) in the presence of different concentrations of LCTR (0.01-10μM) and vascular adhesion molecule (VCAM)-1 expression was evaluated by FACS analysis. As compared with unstimulated cultures, a significant increase in VCAM-1 expression was seen in cells incubated with H (1mM) (p<0.05) but not with TNF-α+IL4. The H-induced VCAM-1 expression was significantly downregulated by LCTR starting at the dose of 0.01μM (p<0.05). Thus, the clinically efficacy of LCTR in patients with in patients with eosinophilic upper airway disorders may include an inhibitory activity on resident fibroblast functions involved in airway inflammation and remodelling.
Supported by UCB Pharma S.p.A.