title: Contribution of interleukin 17A to the development and regulation of allergic inflammation in a murine allergic rhinitis model.
abstract: BACKGROUND
  Interleukin (IL) 17A, a key cytokine of T(H)17 cells, is a well-known proinflammatory cytokine. Despite the important role of T(H)17 cells in acute airway inflammation, the role of IL-17A in allergic rhinitis (AR) remains unclear.
  
  
  OBJECTIVE
  To investigate the role of IL-17A in the allergic response in AR.
  
  
  METHODS
  Wild-type BALB/c and IL-17A-deficient mice were immunized intraperitoneally and were challenged intranasally with ovalbumin. Allergic symptom scores, eosinophil infiltration, serum IgE level, and the levels of several cytokines in nasal lavage fluid and splenocyte supernatants were analyzed.
  
  
  RESULTS
  IL-17A levels increased significantly more in ovalbumin-sensitized wild-type mice than in the negative control group. IL-17A-deficient mice showed a significant decrease in allergic symptoms, serum IgE levels, and eosinophil infiltration into the nasal mucosa compared with wild-type mice. IL-17A-deficient mice also showed decreased histamine and cysteinyl leukotriene release. Bone marrow-derived mast cells from IL-17A-deficient mice showed significantly lower degranulation and secretion of tumor necrosis factor α. Moreover, IL-17A deficiency attenuated the IL-5 level in nasal lavage fluid and its production in response to ovalbumin but did not increase interferon γ production and its level in nasal lavage fluid. In addition, secretion of IL-17A from spleen cells induced the expression of proinflammatory cytokine messenger RNA in macrophages. The mean level of proinflammatory cytokines, including tumor necrosis factor α and IL-17, decreased in IL-17A-deficient mice.
  
  
  CONCLUSIONS
  These results suggest that IL-17A may partly contribute to the development of nasal allergic inflammation in an AR animal model and regulate AR via the activation of proinflammatory cytokines and modulation of T(H)2 cytokine.
authors.affiliation: Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, South Korea.
authors.forename: Song-Hua
authors.initials: SH
authors.lastname: Quan
authors.forename: Yu-Lian
authors.initials: YL
authors.lastname: Zhang
authors.forename: Doo Hee
authors.initials: DH
authors.lastname: Han
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Iwakura
authors.forename: Chae-Seo
authors.initials: CS
authors.lastname: Rhee
mesh_terms: D000818:Animals; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology / Q000503:physiopathology; D007073:Immunoglobulin E / Q000097:blood; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology; D020381:Interleukin-17 / Q000235:genetics / Q000378:metabolism*; D008264:Macrophages; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D009297:Nasal Mucosa / Q000276:immunology; D010047:Ovalbumin / Q000276:immunology; D012220:Rhinitis / Q000276:immunology / Q000503:physiopathology; D018418:Th2 Cells / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D020381:Interleukin-17; D014409:Tumor Necrosis Factor-alpha; D007073:Immunoglobulin E; D010047:Ovalbumin