Abstract
BackgroundNasal polyps of chronic rhinosinusitis (CRS) are characterized by epithelial damage, basement membrane thickness and subepithelial fibrosis. The fibroblast, one of the main cell types making up nasal polyps, is thought to be a target cell of various cytokines. The role of IL-17A in immunoresponse in the nasal poly fibroblast has not yet elucidated.MethodsSubcultured fibroblasts were established from human polyp biopsy tissues in addition to normal mucosal membranes of sphenoid sinuses (controls).ResultsThe IL-17A receptor was expressed at similar levels in all 3 groups. Simultaneous quantification of 27 kinds of cytokines and chemokines in culture supernatants was performed with a human multiplex cytokine assay system. In the eosinophilic group, basal secretion levels of IL-6 were significantly higher than those in the control and non-Eo groups. Basal secretion of MCP-1 in both the non-eosinophilic and eosinophilic groups was also higher than that of the control group. Both IL-9 and G-CSF secretion were remarkably enhanced by IL-17A stimulation in all 3 groups. The receptor-mediated response by IL-17A significantly upregulated IL-6 release alone in the non-eosinophilic and eosinophilic groups as compared with the control group. Only the basic FGF secretion was decreased by stimulation of IL-17A in all groups.ConclusionsOur results demonstrate for the first time a potentially enhanced secretion of IL-6 and MCP-1 from nasal polyp fibroblasts, and a remarkable upregulation of IL-9 and G-CSF from nasal fibroblasts by IL-17A stimulation, which might contribute to nasal polyp formation and airway remodeling.
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