The role of fibroblasts in pathogenesis of bronchial asthma

Abstract

Bronchial asthma is defined as a chronic inflammatory disease of the airways. Nowadays, it is believed that asthma is not a single entity, but a spectrum of diseases (syndrome rather than a disease), that have more or less common pathophysiologic outcomes. In all forms of asthma fibroblasts and other effector cells of the inflammatory response secrete a wide range of preformed and newly generated mediators, which damage the bronchial epithelium, contract smooth muscle and increase mucous secretion. Besides, fibroblasts are of great importance in development of subepithelial fibrosis, smooth muscle hypertrophy and new vessel formation, which lead to the remodelling of airway wall. They also stimulate and modulate inflammation by increasing synthesis of interleukin-8 and monocyte chemotactic proteins. There is ample evidence that oxidants generation is increased during an asthma exacerbation. Fibroblast-derived oxygen metabolites can directly damage a variety of extracellular membrane proteins and/or impair function of antiproteases and/or inactivate enzymes that are involved in elastin synthesis and pulmonary tissue regeneration. However, scientists are still far from the complete understanding of bronchial asthma pathogenesis. Since fibroblasts have been recognized as effector cells capable of inducing pathophysiological features of asthma, there is a hope that further investigations of their role in bronchial asthma pathogenesis will improve treatment of this disease.