Mast cells and airway inflammation in asthma.

A number of new observations have added to our understanding of mast cell biology and the relevance of this cell to the genesis of asthma. The purpose of this review has been to highlight this new information and to refer the reader to extensive reviews where previously documented and well-known data are available. Of particular current interest is the knowledge that mast cell growth and differentiation is regulated by a specific molecule, stem cell factor, which interacts with a receptor on the surface of the mast cell (a tyrosine kinase) and that mast cell phenotype may be modulated by exposure to stem cell factor as well as to a host of inflammatory cytokines. In addition to the ability to release vasoactive/spasmogenic mediators characterized by histamine, the slow-reacting substance of anaphylaxis (sulfidopeptide leukotrienes), platelet-activating factor, and adenosine, the mast cell can release a unique family of enzymes and generate a cassette of cytokines with critically important pro-inflammatory potential. The enzymes that are unique to the mast cell can potentiate a number of inflammatory events central to asthma, including fibroblast activation, mucus secretion, smooth muscle contraction, and neuropeptide degradation, while the cytokines may directly influence the influx, persistence, and activity of inflammatory cells, particularly eosinophilis and basophils, through the ability of the cytokines to modulate endothelial expression of leukocyte adhesion receptors and to prevent target cell apoptosis.(ABSTRACT TRUNCATED AT 250 WORDS)