Abstractfibroblasts, and that the thickness of the subepithelial collagen appears to be Background -Bronchial asthma is charlinked to an increase in bronchial reacterised by airway structural changes, insponsiveness and exacerbation of clinical cluding mucosal inflammatory infiltration manifestations. and subepithelial collagen deposition, that (Thorax 1998;53:21-27) may represent the morphological basis for the chronicity of the disease. The relationship between airway wall thickness Keywords: bronchial asthma, growth factors, fibroblast, remodelling of airway wall.and growth factors in asthma has not been elucidated. Methods -Bronchial biopsy specimens were obtained from 21 asthmatic patients Identification of the histopathological features and eight healthy subjects and the base-of bronchial asthma has been largely based ment membrane thickness was measured on the results of necropsy studies which have by light microscopy and electron micro-documented epithelial cell shedding, inflamscopy. At the same time the numbers of matory cell infiltrate with numerous eosinoeosinophils and fibroblasts were assessed phils, 1 2 and subepithelial collagen thickening. and the expression of transforming growth It has now become clear that this phenomenon factor 1 (TGF-1 ), platelet derived growth occurs in mild atopic asthma, even in patients factor (PDGF), and insulin like growth with a relatively short clinical history.3 In factor (IGF) I in the bronchial mucosa patients with asthma chronic inflammation dewas examined by immunostaining. The termines pathological changes in the airways relationship between the degree of thick-and causes marked remodelling of the structure ening of the subepithelial layer and both of the bronchi. 4 Bronchial biopsy specimens the clinical data and pulmonary function from asthmatic patients have indicated that the were also investigated.typical remodelling of the airways is caused by Results -The basement membrane of the thickening of the subepithelial layer.5 This view asthmatic patients was thicker than that has persisted, despite ultrastructural studies of the healthy controls (median 8.09 versus showing that the true epithelial basement mem-4.02 m). Electron microscopic examina-brane was normal and that the thickening was tion of the basement membrane revealed due to deposition of fibrillar collagen species, thickening of the subepithelial lamina re-leading to an increase in depth and density of ticularis; this thickening significantly cor-the lamina reticularis beneath the basement related with the number of fibroblasts in membrane.6 7 Further studies using antibodies the submucosa in the asthmatic subjects to different types of collagen have revealed an (r S =0.88) but not in the controls (r S =0.70). increase in the amount of interstitial collagen There was a significantly higher number of types I, III, and V and fibronectin in the eosinophils in the airways of the asthmatic thickened basal lamina of patients with subjects than in the healthy subjects asthma. histochemistry. Further...

These findings suggest that inhaled corticosteroid treatment of asthma reduced airway wall vascularity during airway remodelling.