The specialists' view of asthma has evolved from one of a primary disease of the airway re-occurring in an acute and intermittent fashion to that of a chronic, perhaps lifelong inflammatory disorder. Emphasis in research and treatment is shifting away from the symptoms of smooth muscle hyperresponsiveness to the other cells and mediators playing key roles proximal to the emergence and worsening of asthma symptoms. After exposure to antigen a cascade of mediators are elaborated by mast cells, having immediate, but more importantly, late and recurrent effects.
Mediators generateed during mast cell activation are derived in three ways.
These are the release of preformed soluble molecules stored within the mast cell's granules, additional rapidly formed mediators which are formed concurrent to degranulation, and finally molecules with late and prolonged effects made after degranulation. Recent work has also uncovered the synthesis of cytokines, capable of proinflammatory and perhaps immunoregulatory effects as well, by mast cells. A summary of mediatorsreleased with allergic stimulation and their pathophysiologic roles are summarized in Table 1.