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RBM thickness in asthma correlates with the number of myofibroblasts (23) and fibroblasts (24) in the connective tissue and RBM thickness is also associated with a higher number of eosinophils in the bronchial mucosa (25). Thus, RBM thickening is a feature of severe asthma but it has also been described in perennial rhinitis (22). In COPD or in chronic bronchitis, some studies have shown no alteration in RBM thickness compared with healthy control subjects (26); whereas, other studies have shown a slight increase in the thickness compared with controls (18). Increased RBM thickness associated with eosinophils has also been described this website in COPD (6). The smooth muscle mass in the large airways is increased in asthma and there is a relation between the amount and the severity of the disease (27, 28). This increase is because of both hyperplasia and hypertrophia of smooth muscle cells. There is also, however, an increased amount of extracellular matrix components located both within and outside the smooth muscle bundles (29, 30). In fatal asthma, there is a considerable increase in both glands and in smooth muscle bundles, in particular, in the larger bronchi (10). Severe persistent asthma is also associated with higher numbers of fibroblasts, an increase in collagen III, larger mucus glands and smooth muscle cells (27). Even in mild asthmatics, an increase in proteoglycan deposition in the large airways has been described Amiloride (31). It seems that the smooth muscle cells, which are normally located deep in the submucosal tissue, have a much closer location to the epithelium in asthmatics (27). This see more may indicate that a dedifferentiation of smooth muscle cells occur leading to a migration of mesenchymal cells toward the epithelium, thereby supporting the hypotheses of plasticity of structural cells in the airways of asthmatics. In severe asthma, not only the numbers of smooth muscle cells but also the size of the individual cells is increased compared with controls, mild to moderate asthmatics and to patients with COPD. The increase in extracellular matrix components in conjunction with smooth muscle cells in asthma may affect airway wall compliance, resulting in a more ��stiff�� tissue and limit the smooth muscle cell-induced airway narrowing (29). In COPD, there is no such increase in smooth muscle bundles in the large airways, although some earlier studies have shown slightly more smooth muscle compared with controls (2, 29). Remodeling of the small (