The Effect of Azelastine on the Infiltration of Inflammatory Cells into the Bronchial Mucosa and Clinical Changes in Patients with Bronchial Asthma

Abstract

Background: Azelastine is an oral antiallergic compound but there is no direct evidence of its anti-inflammatory actions in bronchial asthma. We examined the effect of azelastine on inflammatory cells infiltrating the bronchial mucosa and clinical symptoms in atopic asthma in a double-blind, parallel, randomized study. Methods: The study was completed by 13 subjects in the azelastine (4 mg/day) group and 11 subjects in the placebo group. Treatments were randomly administered for 3 months. Each subject recorded daily asthma symptoms and peak expiratory flow (PEF). Lung function and bronchial responsiveness to methacholine were measured before and after treatment. Fiberoptic bronchoscopy was performed and bronchial biopsies taken from segmental carinae before and after treatment with azelastine or placebo. Using each monoclonal antibody for eosinophils, mast cells, macrophages, and T lymphocytes we performed immunohistological staining on biopsy specimens. Results: Compared with the placebo-treated group, the azelastine-treated group exhibited significant improvement of asthma symptoms (p < 0.01), PEF (p < 0.01), PEF diurnal variation (p < 0.001), excluding forced expiratory volume in 1 s or airway responsiveness. This was accompanied by a reduction of EG2(+) eosinophils (p < 0.01), CD3(+) (p < 0.001), CD4(+) (p < 0.05), CD8(+) (p < 0.05) T lymphocytes, and CD25(+)-activated T lymphocytes (p < 0.001) in the bronchial mucosa. Significant correlations were found between clinical data and immunohistochemical parameters. Conclusion: These results demonstrated that the beneficial effects of azelastine in bronchial asthma may result from modulation of local bronchial inflammatory cell infiltration.

Differential Effect of Antiallergic Drugs on IgE-Mediated Cutaneous Reaction in Passively Sensitized Mice

“…However, azelastine, although classified as a basic compound along with terfenadine, inhibited both IPR and LPR. In addition to the inhibition of mediator production and release, azelastine has been shown to inhibit the generation of superoxide from activated neutrophils [5], and to reduce the infiltration of eosinophils and activated T lymphocytes into the bronchial mucosa in patients with asthma [12]. Azelastineinduced inhibition of LPR may be partly associated with the direct effect against inflammatory cells, although the precise mechanism remains to be examined in detail.…”

Allergic eye disease mechanisms

“…Of the new generation of H 1 receptor antagonists, topical azelastine has been shown to be a powerful topical antihistamine, decreasing eosinophils and T lymphocyte activation 108. It both reduces and prevents the symptoms of SAC,109 but does not appear to reach maximal activity for 7 days 110.…”

The anti‐inflammatory effects of the second‐generation antihistamines

“…A similar study also concluded that cetirizine could prevent exacerbation of seasonal pollen asthma (48). Azelastine treatment of 13 asthmatic patients resulted in significant improvement in asthma symptoms accompanied by a reduction in activated eosinophils and T lymphocytes in the bronchial mucosa compared with the placebo‐treated group (49), while another study found that azelastine reduced the need for inhaled corticosteroids in patients with chronic bronchial asthma (50). In addition, azelastine treatment of patients with chronic asthma resulted in rapid onset of bronchodilating activity, as demonstrated by a statistically significant mean percentage improvement in FEV 1 (51).…”