title: Expression and regulation of interleukin-9 in chronic rhinosinusitis.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Otorhinolaryngology, Eye and Ear, Nose, and Throat Hospital of Fudan University, Shanghai, China.
authors.forename: Hai
authors.initials: H
authors.lastname: Lin
authors.forename: Dong
authors.initials: D
authors.lastname: Lin
authors.forename: Xi-Sheng
authors.initials: XS
authors.lastname: Xiong
authors.forename: Xiong-Xiong
authors.initials: XX
authors.lastname: Dai
authors.forename: Ting
authors.initials: T
authors.lastname: Lin
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002908:Chronic Disease; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D016906:Interleukin-9 / Q000032:analysis* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009297:Nasal Mucosa / Q000276:immunology; D012333:RNA, Messenger / Q000032:analysis; D053651:Receptors, Interleukin-9 / Q000032:analysis / Q000235:genetics; D012220:Rhinitis / Q000276:immunology*; D012852:Sinusitis / Q000276:immunology*
chemical_list: C508607:IL9 protein, human; D016906:Interleukin-9; D012333:RNA, Messenger; D053651:Receptors, Interleukin-9