Abstract
The mast cell has long been considered to be of paramount importance in the pathophysiology of asthma. Its key role in driving the IgE-mediated allergic reaction and thus the early asthmatic response is well documented. In addition, there is evidence that it responds to non-IgE stimuli in the airway — for example, changes in the osmotic cellular environment associated with such challenges as exercise, hypertonicity, and hypotonicity. The array of mediators released from the activated mast cell is diverse, including prostaglandins; leukotrienes; cytokines, such as interleukins 1, 2, 4, 10, and 13; growth factors, such as platelet-derived growth factor and . . .