Tobacco is an important etiologic factor in the development of COPD, and is considered an aggravating factor in a number of interstitial lung diseases. In general, these pulmonary disorders are characterized by inflammation and the activation of tissue remodeling that result in structural alterations such as airway wall thickening and the destruction of alveolar septae. Corticosteroids are commonly used in the treatment of these disorders Viagra medstore, and their beneficial effects are often ascribed to their anti-inflammatory properties. More recently, attention has been given to the potential effects of corticosteroids on tissue remodeling. For example, inhalation of the corticosteroid fluticasone propionate (FP) was found to partially inhibit airway wall thickening and matrixdeposition in a rat model of allergen-induced airway remodeling, and limited the progression of structural airway changes in this model. These studies suggest that corticosteroids might ameliorate progressive tissue remodeling in diseases characterized by airflow obstruction, but the mechanisms responsible for this effect remain unelucidated. We speculate that corticosteroids might inhibit lung tissue remodeling by directly modulating the expression of extracellular matrix genes in lung fibroblasts.
In an attempt to elucidate the effects of corticosteroids on extracellular matrix gene expression, we studied the expression of fibronectin in fibroblasts treated Sildenafil online with FP. Fibronectin is an extracellular matrix glycoprotein that is highly expressed in acute and chronic forms of lung injury including COPD, asthma, and many interstitial lung diseases. Villiger et al demonstrated an increase in the production of fibronectin in alveolar macrophages obtained from smokers when compared to nonsmokers. Alveolar macrophages from patients with chronic bronchitis spontaneously released greater amounts of fibronec-tin than those from asthmatic patients and control subjects. The levels of fibronectin have been correlated with a decrease in pulmonary function in smokers with COPD. In asthma, airway wall remodeling is not only associated with increased deposition of extracellular matrices, but also with alterations in the composition of the airway wall connective tissue with increased deposition of fibronectin. The aforementioned studies have implicated excessive production of fibronectin as a marker of activation of tissue remodeling and a potential mechanism for promoting fibroproliferation in tobacco-related lung disease.