Airway inflammation is an integral component of asthma. A subtype of lymphocytes (Th2 cells) has been demonstrated in airways of asthma subjects. These cells are capable of secreting a defined profile of cytokines which have the capacity to activate airway inflammatory cells such as eosinophils. We hypothesize that in allergic subjects allergen challenge leads to stimulation of Th2 cells to release cytokines that activate inflammatory cells by cytokines causing airway inflammation and injury. We further hypothesize, that antigen-induced airway inflammation is more persistent in patients with allergic asthma compared to those with allergic rhinitis. This persistence of this inflammation in allergic asthmatics contributes to airway hyperresponsiveness and obstruction. To test this hypothesis we propose the following specific aims: 1) to determine the differences in persistence of antigen-induced airway eosinophilia between allergic asthmatic and allergic rhinitis subjects, 2) to determine the expression of IL-5 in BAL fluid and airway cell culture supernatants between allergic rhinitis and allergic asthmatic subjects, and 3) To examine the relationship between airway cell capacity to generate IL-5 and the degree (and persistence) of airway eosinophilia post antigen challenge. """"""""
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