title: Interleukin-17A-induced inflammation does not influence the development of nasal polyps in murine model.
abstract: BACKGROUND
  Nasal polyposis associated with chronic rhinosinusitis (CRS) is a chronic inflammatory disease that is characterized by infiltration of many inflammatory cells. Meanwhile, interleukin (IL)-17A is a well-known proinflammatory cytokine that induces both eosinophilic and neutrophilic inflammation. We investigated the role of IL-17A in the development of nasal polyps in the CRS murine model.
  
  
  METHODS
  Eosinophilic CRS with nasal polyps was induced by using ovalbumin (OVA) and Staphylococcus aureus enterotoxin B (SEB) in wild-type BALB/c and IL-17A knockout (KO) mice. Histopathologic changes of the sinonasal cavity were evaluated using hematoxylin and eosin, Periodic acid-Schiff, Sirius red, Masson's trichrome, and immunohistochemistry. The levels of total and OVA-specific immunoglobulin Es (IgEs) in sera were measured using enzyme-linked immunosorbent assay. The expression levels of IL-4, IL-5, and interferon-γ (IFN-γ) in the nasal mucosa were assessed by quantitative real-time polymerase chain reaction.
  
  
  RESULTS
  Under the IL-17A deficiency, total and OVA-specific IgEs in sera were reduced significantly. Infiltration of both eosinophils and neutrophils into the nasal mucosa, subepithelial fibrosis, and goblet cell count also decreased significantly in IL-17A KO mice treated with both OVA and SEB compared with those in the wild-type counterpart. However, there were no significant differences in the number of polypoid lesions among groups. Meanwhile, IL-4 increased and IFN-γ decreased in the nasal mucosa in IL-17A KO mice treated with both OVA and SEB.
  
  
  CONCLUSIONS
  This study suggests that even though IL-17A plays an important role in both nasal inflammation and remodeling, it does not influence the development of nasal polypoid lesions.
authors.affiliation: Department of Otorhinolaryngology-Head and Neck Surgery, Pusan National University Hospital, Busan, South Korea.|Medical Research Institute, Pusan National University Hospital, Busan, South Korea.|Graduate School of Immunology, Seoul National University College of Medicine, Seoul, South Korea.
authors.forename: Sung-Lyong
authors.initials: SL
authors.lastname: Hong
authors.affiliation: Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, South Korea.
authors.forename: Yu-Lian
authors.initials: YL
authors.lastname: Zhang
authors.affiliation: Department of Otorhinolaryngology, Gyeongsang National University, Jinju, South Korea.
authors.forename: Sang-Wook
authors.initials: SW
authors.lastname: Kim
authors.affiliation: Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, South Korea.|Department of Otorhinolaryngology, Seoul National University Boramae Medical Center, Seoul, South Korea.
authors.forename: Dae Woo
authors.initials: DW
authors.lastname: Kim
authors.affiliation: Graduate School of Immunology, Seoul National University College of Medicine, Seoul, South Korea.|Department of Internal Medicine, Seoul National University Hospital, Seoul, South Korea.
authors.forename: Sang-Heon
authors.initials: SH
authors.lastname: Cho
authors.affiliation: Department of Internal Medicine, Seoul National University Bundang Hospital, Gyeonggi, South Korea.
authors.forename: Yoon-Seok
authors.initials: YS
authors.lastname: Chang
authors.affiliation: Department of Otorhinolaryngology, Seoul National University College of Medicine, Seoul, South Korea.|Department of Otorhinolaryngology, Seoul National University Bundang Hospital, Gyeonggi, South Korea.
authors.forename: Chul Hee
authors.initials: CH
authors.lastname: Lee
authors.affiliation: Graduate School of Immunology, Seoul National University College of Medicine, Seoul, South Korea.|Department of Otorhinolaryngology, Seoul National University Bundang Hospital, Gyeonggi, South Korea.|Research Center for Sensory Organs, Seoul National University Medical Research Center, Seoul, South Korea.|Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea.
authors.forename: Chae-Seo
authors.initials: CS
authors.lastname: Rhee
mesh_terms: D000818:Animals; D002908:Chronic Disease; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000378:metabolism; D020381:Interleukin-17 / Q000502:physiology*; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D009297:Nasal Mucosa / Q000378:metabolism; D009298:Nasal Polyps / Q000378:metabolism* / Q000473:pathology; D060888:Real-Time Polymerase Chain Reaction; D012220:Rhinitis / Q000378:metabolism* / Q000473:pathology; D012852:Sinusitis / Q000378:metabolism* / Q000473:pathology
chemical_list: C508717:IL17A protein, human; D020381:Interleukin-17; D015848:Interleukin-5; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma
keywords: Staphylococcal enterotoxin B; airway remodeling; inflammation; interleukin-17A; nasal polyps