title: Expression of IL-16 in allergen-induced late-phase nasal responses and relation to topical glucocorticosteroid treatment.
abstract: Allergen-induced late nasal responses (LNRs) are associated with a cellular infiltrate in which CD4+ cells are prominent. These cells have been shown to be the major cellular source of Th2-type cytokines. Mechanisms responsible for the local accumulation of CD4+ cells in the nasal mucosa after allergen exposure are unclear. IL-16 is a potent chemoattractant for CD4+ cells in vitro and may play a significant role in recruiting CD4+ cells in LNRs. We investigated the expression of IL-16 messenger RNA and immunoreactivity in nasal biopsy specimens from 17 subjects with allergic rhinitis. A biopsy specimen of the nasal inferior turbinate was obtained before and 24 hours after local nasal provocation with grass pollen extract after 6 weeks of treatment with either topical fluticasone propionate (n = 9) or placebo (n = 8) nasal spray twice daily. IL-16 mRNA-positive cells and IL-16-immunoreactive cells were identified in both the epithelium and the subepithelial tissue at baseline. Within the placebo-treated group, the numbers of epithelial and subepithelial IL-16 mRNA-positive cells and IL-16-immunoreactive cells were significantly increased 24 hours after challenge compared with baseline (p < 0.001). Topical glucocorticoid therapy resulted in a decrease in allergen-induced epithelial immunoreactive cells and subepithelial IL-16 mRNA-positive cells. The numbers of CD4+ cells increased after antigen challenge compared with baseline (p < 0.05), and this increase was inhibited by glucocorticoid treatment. There were significant correlations between epithelial and subepithelial IL-16 immunoreactivity and CD4+ cell infiltration after antigen challenge. The upregulation of IL-16 expression in allergic nasal mucosa after antigen challenge may have critical implications in the accumulation of CD4+ cells in response to antigen exposure. Steroid-mediated inhibition of IL-16 may be partly responsible for the decrease in local CD4+ cells after topical glucocorticoid therapy.
authors.affiliation: Meakins-Christie Laboratories, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
authors.forename: S
authors.initials: S
authors.lastname: Laberge
authors.forename: S R
authors.initials: SR
authors.lastname: Durham
authors.forename: O
authors.initials: O
authors.lastname: Ghaffar
authors.forename: S
authors.initials: S
authors.lastname: Rak
authors.forename: D M
authors.initials: DM
authors.lastname: Center
authors.forename: M
authors.initials: M
authors.lastname: Jacobson
authors.forename: Q
authors.initials: Q
authors.lastname: Hamid
mesh_terms: D000287:Administration, Topical; D000485:Allergens / Q000276:immunology* / Q000494:pharmacology; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001706:Biopsy; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D004311:Double-Blind Method; D004848:Epithelium / Q000378:metabolism; D005938:Glucocorticoids; D006801:Humans; D019410:Interleukin-16 / Q000096:biosynthesis* / Q000276:immunology; D009297:Nasal Mucosa / Q000187:drug effects* / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D006255:Rhinitis, Allergic, Seasonal / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism*
chemical_list: D000485:Allergens; D000893:Anti-Inflammatory Agents; D005938:Glucocorticoids; D019410:Interleukin-16; D012333:RNA, Messenger