What is asthma? An update on the mechanisms.

Asthma is currently best described by the presence of characteristic symptoms and by variable airways narrowing and airways hyperresponsiveness to a variety of inhaled bronchoconstricting stimuli. For more than 100 years, asthma has also been known to be an inflammatory disease of the airways. More recently, the importance of airways inflammation in the pathogenesis of asthma, ranging in severity from mild to severe, or in transient asthma after exposure to an inflammatory stimulus, has been recognized. Airways inflammation can be defined as the presence of activated inflammatory cells in the airways. Many studies have now demonstrated the presence of activated eosinophils and of mast cells in the airways lumen and airways wall of patients with asthma, even those with mild disease. The presence and survival of these inflammatory cells may be promoted by the presence of increased levels of proinflammatory cytokines, such as GM-CSF, in asthmatic airways. These cells have the capacity to release potent bronchoconstricting mediators, such as the cysteinyl leukotrienes, which are responsible, at least in part, for airways narrowing in asthma and for allergen-, exercise- and aspirin-induced asthma. Other cells, such as a subset of T-lymphocytes (Th2), may also be important in maintaining the inflammatory cascade. Airways structural changes caused by persisting inflammation, such as airways epithelial damage, or altered smooth muscle function or volume are likely to be important in the pathogenesis of stable, long-standing airways hyperresponsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)