Literature DB >> 9338554

Expression of IL-16 in allergen-induced late-phase nasal responses and relation to topical glucocorticosteroid treatment.

S Laberge1, S R Durham, O Ghaffar, S Rak, D M Center, M Jacobson, Q Hamid.   

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.

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Year:  1997        PMID: 9338554     DOI: 10.1016/s0091-6749(97)70152-0

Source DB:  PubMed          Journal:  J Allergy Clin Immunol        ISSN: 0091-6749            Impact factor:   10.793


  8 in total

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4.  Interleukin-16 inhibits interleukin-13 production by allergen-stimulated blood mononuclear cells.

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Review 6.  Regulation of allergic airways inflammation by cytokines and glucocorticoids.

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7.  Inflammatory patterns of allergic and nonallergic rhinitis.

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8.  The release of IL-31 and IL-13 after nasal allergen challenge and their relation to nasal symptoms.

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  8 in total

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