Asthma is a chronic inflammatory disease characterized by varying degrees of airflow obstruction and diverse clinical manifestations. As knowledge of asthma pathogenesis has increased, treatment has evolved. Airway inflammation, modulated by genetic and environmental factors, results in altered airway architecture (airway remodeling). Inflammation in asthma is typically multicellular in nature, involving mast cells, neutrophils, eosinophils, and T lymphocytes, as well as muscle and epithelial cells. Various cytokines and chemokines play roles in orchestrating the inflammatory process. Recognition of the critical role played by airway inflammation, which is an indicator of the degree of asthma severity, has shifted the treatment toward either prevention or the inhibition of inflammatory markers. In light of this, new drug formulations have been considered. In addition to the beta2 agonists, theophylline, and corticosteroids currently being used, the second generation of selective phosphodiesterase inhibitors has shown promising results. Recent studies suggest that these drugs may soon offer a novel alternative in the treatment of asthma.
Phosphodiesterase inhibitors; Inflammation mediators; Asthma