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.