BACKGROUND: The pathogenesis of human chronic rhinosinusitis (CRS) remains controversial. Recent evidence has suggested that interleukin (IL)-9 is vital in eliciting inflammatory response, stimulating cell proliferation and preventing apoptosis, through binding to the IL-9 receptor (IL-9R). However, little is known about the roles of both molecules in the etiology of CRS. Therefore, this study aimed to assess IL-9 and IL-9R expression and determine their roles in the pathophysiology of CRS. METHODS: Immunohistochemistry was used to assess IL-9 and IL-9R immunolabeling. In addition, Western blotting and real-time polymerase chain reaction (PCR) were used for IL-9 and IL-9R protein and mRNA level quantitation, respectively, in CRS and control subjects. Furthermore, the effects of various stimulators at different concentrations and time on IL-9 were evaluated using nasal explant cultures. RESULTS: IL-9 and IL-9R were overexpressed in CRS, especially in CRS with nasal polyps. Interestingly, IL-9 expression was closely related to that of IL-9R. In addition, IL-9 mRNA levels were increased by treatment with IL-4, IL-17A, IL-1beta, and the IL-4 and transforming growth factor (TGF) beta1 combination, but suppressed by interferon gamma and IL-27. CONCLUSION: IL-9 and IL-9R were overexpressed in CRS at both protein and mRNA levels. In addition, IL-4, IL-17A, IL-1beta, and the IL-4 and TGF-beta1 combination contributed to increased IL-9 levels. Our findings indicate that IL-9 may play a proinflammatory role after IL-9R binding to induce mucosal epithelial cell growth, gland epithelial cell proliferation, and inflammatory cell infiltration in CRS. Future studies are required to further define the role of IL-9 in CRS etiology.
BACKGROUND: The pathogenesis of humanchronic rhinosinusitis (CRS) remains controversial. Recent evidence has suggested that interleukin (IL)-9 is vital in eliciting inflammatory response, stimulating cell proliferation and preventing apoptosis, through binding to the IL-9 receptor (IL-9R). However, little is known about the roles of both molecules in the etiology of CRS. Therefore, this study aimed to assess IL-9 and IL-9R expression and determine their roles in the pathophysiology of CRS. METHODS: Immunohistochemistry was used to assess IL-9 and IL-9R immunolabeling. In addition, Western blotting and real-time polymerase chain reaction (PCR) were used for IL-9 and IL-9R protein and mRNA level quantitation, respectively, in CRS and control subjects. Furthermore, the effects of various stimulators at different concentrations and time on IL-9 were evaluated using nasal explant cultures. RESULTS:IL-9 and IL-9R were overexpressed in CRS, especially in CRS with nasal polyps. Interestingly, IL-9 expression was closely related to that of IL-9R. In addition, IL-9 mRNA levels were increased by treatment with IL-4, IL-17A, IL-1beta, and the IL-4 and transforming growth factor (TGF) beta1 combination, but suppressed by interferon gamma and IL-27. CONCLUSION:IL-9 and IL-9R were overexpressed in CRS at both protein and mRNA levels. In addition, IL-4, IL-17A, IL-1beta, and the IL-4 and TGF-beta1 combination contributed to increased IL-9 levels. Our findings indicate that IL-9 may play a proinflammatory role after IL-9R binding to induce mucosal epithelial cell growth, gland epithelial cell proliferation, and inflammatory cell infiltration in CRS. Future studies are required to further define the role of IL-9 in CRS etiology.