Until recently, asthma therapy focused on acute treatment of such attacks with bronchodilator therapy; however, it is now known that the degree of underlying inflammation does not result in acute bronchospasm, but it modifies the biology of the airway in such a way as to cause bronchial hyperresponsiveness Holgate and Pauwels (2000:9)
An allergen may trigger the release of a host of cellular mediators, cytokines and chemokines from a variety of inflammatory cells, which results in increased smooth muscle responsiveness. Empirical observations also support the role of underlying inflammation as a cause of airway hyperresponsiveness "the presence of inflammation is correlated with hyperresponsiveness and the use of anti-inflammatory drugs decreases hyperresponsiveness Bush and Georgitis (1997:37). .
While an asthma "attack" is an acute event in which lung function may return to normal, chronic asthma can lead to lung remodelling and permanent changes in lung function. Increased bronchial vascular permeability leads to chronic airway oedema which in turn leads to mucosal thickening and swelling of the airway. Increased mucus secretion and viscosity may plug airways, leading to airway obstruction. Changes in the extracellular matrix in the airway wall may also lead to permanent obstruction. .
Leukotrienes are among the molecules released in response to various asthma triggers. These molecules are formed by the action of 5-lipoxygenase on arachidonic acid and are produced by mast cells, eosinophils and alveolar macrophages Holgate and Pauwels (2000:10). Leukotrienes are responsible, in part, for increased mucus production, bronchoconstriction and eosinophil infiltration observed in asthma. The complex role of leukotrienes in asthma, and the availability of highly effective leukotriene inhibitors, offer expanded treatment options to the widely accepted model of asthma as a condition with an inflammatory and a bronchoconstrictive component that should be managed by inhaled corticosteroids and bronchodilators Hyland (1998:18).
