OBSERVATIONS ON THE RESPONSE OF THE NASAL-MUCOSA TO ALLERGENS

Allergic rhinitis is the sixth most prevalent chronic health condition in the United States. To study the pathogenesis of the allergic respo nse, we have used a model of nasal provocation with antigen. During th e initial reaction of an allergic subject to allergen provocation, inc reases occur in the levels of histamine, tryptase, and prostaglandin D -2. This pattern of mediator release, combined with histologic evidenc e of mast-cell degranulation, strongly supports the role of the mast c ell in the acute allergic reaction. The response to antigen, however, does not end with mast-cell degranulation. Hours after challenge we ob served the spontaneous recurrence of symptoms and increased responsive ness to antigenic and nonantigenic stimuli. Our central hypothesis is that cellular infiltration and activation after antigen challenge are responsible for the observed Increase in nasal reactivity. The predomi nant cells in nasal lavage 24 hours after challenge are eosinophils an d neutrophils, whereas the predominant cell in the mucosa is the CD4() lymphocyte. An early step in the movement of cells from the peripher al blood involves adhesion between circulating leukocytes and the endo thelium. Evidence suggests that vascular endothelial adhesion molecule may be responsible in part for the selective adherence of eosinophils to the endothelium.