571 Clinical and Laboratory Studies of the Fate of Intranasal Allergen

Abstract

BackgroundThe nose is generally the first site of contact for inhaled particles including allergen, however the precise way in which allergen is handled by the nose is unknown.ObjectiveThis study aimed to describe the dispersal of Der p 1 allergen by measuring the recovery of allergen following nasal administration and to evaluate whether Der p 1 can be detected in nasal biopsies after natural exposure and nasal challenge.MethodsDer p 1 allergen was administered intranasal to 20 non-atopic healthy subjects and recovery of Der p 1 was measured in the nasal wash, nasal mucus and induced sputum up to 30 minutes after challenge.In 8 subjects (5 atopics) Der p 1 was sprayed intranasal into one nostril and 30 minutes later a biopsy was taken, the contralateral nostril served as a negative control. Immunohistological localisation of Der p 1, IgE positive cells, macrophages was undertaken. Eosinophils were shown by H-E staining.Results1) Less than 25% of total allergen inserted into the nasal cavity was retrievable after aqueous or particulate allergen challenge. Most allergen was retrieved from the nasal mucus.Under baseline conditions, in atopics and non-atopics, mild Der p 1 tissue staining in nasal epithelial tissue was observed. Following challenge epithelial Der p 1 staining increased both in atopics and non-atopics, while increased staining of lamina propria was found in atopics only. Also increased eosinophils, macrophages and IgE positive cells were observed in areas of higher concentrations of Der p 1 staining in the epithelium, mucous glands and lamina propria compared to the contralateral unchallenged nasal mucosa and also compared to the nonatopics.ConclusionsDer p 1 allergen is detected in nasal tissue after natural exposure and independent of atopic status. After challenge the nose effectively retains allergen which is mucosally located. Furthermore in atopics allergen is bound to epithelial cells and rapidly transported to the subepithelial lamina propria where it can bind to IgE-bearing mast cells and recruit eosinophils and macrophages facilitating induction and persistence of inflammation.