Regular albuterol or nedocromil sodium - effects on airway subepithelial tenascin in asthma

Citation
A. Altraja et al., Regular albuterol or nedocromil sodium - effects on airway subepithelial tenascin in asthma, RESP MED, 93(7), 1999, pp. 445-453
Citations number
39
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
RESPIRATORY MEDICINE
ISSN journal
09546111 → ACNP
Volume
93
Issue
7
Year of publication
1999
Pages
445 - 453
Database
ISI
SICI code
0954-6111(199907)93:7<445:RAONS->2.0.ZU;2-D
Abstract
Both albuterol and nedocromil sodium have been recognized to possess certai n anti-inflammatory properties. However, there are no data on the impact of these drugs on the pathophysiology of the bronchial extracellular matrix i n asthma characterized by enhanced tenascin (Tn) expression, known to occur proportional to the severity of asthma. This paper reports data from a mor phometric study on the effects of regular treatment with inhaled albuterol or nedocromil sodium on the extent of bronchial subepithelial deposition of Tn, collagen types III, IV, and VII and mucosal infiltration with macropha ges. Thirty-two patients (14 women) with chronic asthma, aged 38.7 years (median ) with a median forced expiratory volume in 1 sec (FEV1) of 74.4% predicted , were selected to undergo fibre-optic bronchoscopy with bronchial biopsies before and after 12 weeks of treatment with either inhaled albuterol 0.2 m g or nedocromil sodium 4 mg four times daily according to a double-blind pr otocol. Cryostat sections of the biopsy specimens were studied by indirect immunostaining techniques using monoclonal antibodies and computer-assisted quantitative image analysis. Albuterol treatment significantly reduced the median thickness of subepithe lial Tn expression from 9.7 to 6.3 mu m (P=0.023) and macrophage numbers in the epithelium (P=0.034), lamina propria (P=0.039) and entire mucosa (P=0. 033), whereas nedocromil sodium had no effect. Expression of the collagen t ypes was not affected by either treatment. There was no identifiable statis tical difference between the two treatments for any of the outcome variable s measured. Nevertheless, the results demonstrate that even a short-acting beta(2)-agonist may exert antiinflammatory potential sufficient to interfer e with the basic mechanisms of asthma as shown by reduction of subepithelia l Tn content and mucosal macrophage count.