Nasal IL-16 and MIP-1 alpha in late-phase allergic response.

Abstract

Late-phase response in allergic rhinitis is characterized by tissue eosinophilia and influx of CD4+ T-cells. IL-16 and MIP-1 alpha are highly chemotactic on T-cells and on eosinophils. Both IL-16 and MIP-1 alpha have been demonstrated to be up-regulated after challenge in the late-phase response in various atopic conditions other than allergic rhinitis. The aim of our study was to determine the expression of IL-16 and MIP-1 alpha in nasal secretions following allergen challenge in allergic rhinitis, and to compare these with characteristic late-phase mediators such as IL-5 and ECP. Nasal secretions of 14 allergic volunteers challenged intranasally by their specific allergen were studied from 20 minutes to 8 hours after allergen challenge. Nasal secretions were analyzed by routine ELISA for IL-16, MIP-1 alpha, IL-5, and ECP. IL-16 and MIP-1 alpha increased significantly in nasal secretions of challenged allergic patients in the late-phase response. IL-16 revealed highest amounts 5 hours after challenge, whereas MIP-1 alpha peaked at 7 hours. Both correlated significantly (r = 0.917, p < 0.05) at 6 hours. IL-5 and ECP peaked between 6 and 8 hours and correlated significantly (r = 0.951, p < 0.01) at 6 hours as well. Our data demonstrate that IL-16 and MIP-1 alpha are expressed in the late-phase response in allergic rhinitis in a more or less similar kinetic like IL-5 and ECP. They are suggested to be responsible for the observed influx of eosinophils (IL-5, IL-16, and MIP-1 alpha) and CD4+ T-cells (IL-16 and MIP-1 alpha) into the challenged allergic mucosa.