[Contemporary views on the pathological mechanism of asthma]

Asthma is a chronic inflammatory disease of the airways. Genetic and environmental factors contribute to the development of asthma. Both inflammation and remodelling are essential mechanisms in the development of subepithelial fibrosis and smooth muscle hypertrophy leading to progressing decrease of FEV1. Inflammatory changes in asthma are characterised by cellular infiltration of airway epithelium, bronchial wall and smooth muscle layer. The most important cells participating in asthma include T lymphocytes, mast cells, airway epithelial cells, eosinophils, antigen-presenting cells, neutrophils, fibroblasts, myofibroblasts and macrophages. They produce many cytokines responsible for the development of allergen-specific clones of Th2 lymphocytes, for production of IgE by B-cells, for increased expression of adhesion molecules, for migration of cells, their activation and release of inflammatory mediators. The mediators coming mainly from mast cells and eosinophils that include leukotrienes, prostaglandins, histamine, alkaline proteins and enzymes are responsible for airway obturation that results from bronchospasm, bronchial mucosal oedema and excessive amount of abnormal mucous secretion. An important role in the obturation is played by smooth muscle hypertrophy and deposition of proteins under the basal membranes of respiratory epithelium.