EXPRESSION OF IL-16 IN ALLERGEN-INDUCED LATE-PHASE NASAL RESPONSES AND RELATION TO TOPICAL GLUCOCORTICOSTEROID TREATMENT

Allergen-induced late nasal responses (LNRs) are associated with a cel lular infiltrate in which CD4(+) cells are prominent. These cells have been shown to be the major cellular source of Th2-type cytokines. Mec hanisms responsible for the local accumulation of CD4(+) cells in the nasal mucosa after allergen exposure are unclear. IL-16 is a potent ch emoattractant for CD4(+) cells in vitro and may play a significant rol e in recruiting CD4(+) cells in LNRs. We investigated the expression o f IL-16 messenger RNA and immunoreactivity in nasal biopsy specimens f rom 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) nasa l spray twice daily. IL-16 mRNA-positive cells and IL-16-immunoreactiv e cells were identified in both the epithelium and the subepithelial t issue at baseline. Within the placebo-treated group, the numbers of ep ithelial and subepithelial IL-16 mRNA-positive cells and IL-16-immunor eactive cells were significantly increased 24 hours after challenge co mpared with baseline (p < 0.001). Topical glucocorticoid therapy resul ted in a decrease in allergen-induced epithelial immunoreactive cells and subepithelial IL-16 mRNA-positive cells. The numbers of CD4(+) cel ls increased after antigen challenge compared with baseline (p < 0.05) , and this increase was inhibited by glucocorticoid treatment. There w ere significant correlations between epithelial and subepithelial IL-1 6 immunoreactivity and CD4(+) cell infiltration after antigen challeng e. 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 inhi bition of IL-16 may be partly responsible for the decrease in local CD 4(+) cells after topical glucocorticoid therapy.