[Pathogenesis of bronchial asthma--unveiling new therapeutic prospects]

Bronchial asthma is a chronic inflammatory disease of the lower respiratory tract. It is characterized by nonspecific bronchial hyperresponsiveness, which may lead to variable, reversible airflow obstruction in affected patients. Despite therapeutic improvements, the worldwide prevalence and morbidity of asthma have risen during the past decades. An improved understanding of underlying pathological features and mechanisms of asthmatic inflammation is essential to achieve an enhanced asthma symptom control and may lead to prevention in the future.

Besides the impact of genetic and environmental factors, scientific interest has especially been focused on the molecular and cellular biology of the asthmatic response. Mucosal inflammation in asthmatics is mainly orchestrated by T cells and derived cytokines. Immunoglobulin E and mast cells play a pivotal role in the initiation and pathogenesis of the early asthmatic reaction, while recruitment and activation of eosinophils seem to be crucial for the persistent asthma phenotype with chronic airflow obstruction. Additionally, smooth muscle cells, parasympathetic nerve fibers, bronchial epithelial cells and a vast amount of mediators may either promote or inhibit the inflammatory pathology of bronchial asthma.

The recent insights from molecular biology have found their correlate in actual therapeutic guidelines, and have further led to the development of new innovative asthma drugs such as monoclonal antibodies against IgE or IL-5. Hopefully, future progress in revealing pathogenetic mechanisms of asthma may lead to further therapeutic improvement and eventually reverse the trend of rising asthma morbidity in western societies.