[Bronchial asthma--a chronic inflammatory disorder].

Inflammation is a major process in the pathogenesis of bronchial asthma. Pivotal role in the induction of the inflammation in atopic subjects is played by mast cells and eosinophils and their mediators. Lymphocytes T and macrophages modulate this process. Although the pathogenesis of asthma in non-atopic subjects is not totally clear the inflammation has similar course as in asthma with IgE overproduction. Current research emphasise e.g. the role of adhesion molecules, bronchial epithelial cells and nitric oxide in the pathogenesis of asthma. Selectin E, ICAM-1, VCAM-1 take part in the migration of inflammatory cells in the asthmatic lung. Expression of these molecules is included by IL-1, TNF-alpha, and IL-4. Inflammation leads to the bronchial epithelial damage and release of proinflammatory cytokines, which augment the above process. The epithelial damage causes exposure of nerve endings, which can lead to the activation of axon reflexes. The concentration of NO in the exhaled air of asthmatics is much higher than in healthy subjects. It may be produced by inflammatory cells and may augment the inflammation as well as cause bronchial hyperresponsiveness. The better understanding of inflammatory patterns of bronchial asthma has major influence on the therapeutic approach. Inhaled anti-inflammatory drugs are of the first choice in pharmacotherapy of even mild forms of asthma.