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. (J Allergy Clin Immunol 1997;100:569-74.)