ABSTRACT
The exact mechanisms underlying airway hyperresponsiveness are incompletely known, but likely involve a variety of factors including baseline airway geometry, autonomic nervous control of the smooth muscle, the smooth muscle cell itself, bronchial mucosal permeability, and epithelial damage and inflammation. Evidence that mast cells contribute to airway contraction in asthma comes from both in vitro and in vivo studies. The growing appreciation of the diverse consequences of mast cell degranulation has led to an expanding list of mediators produced by this event. Histamine and serotonin are biogenic amines found in mast cells. Human mast cells contain two major neutral proteases, tryptase and chymase, which represent the major protein component of these cells. The potential role of inflammatory cells and inflammation in the pathogenesis of asthma is illustrated by a number of observations. A high-molecular-weight neutrophil chemotactic factor of presumptive mast cell origin has also been described.
