title: Expression of IL-33 and its receptor ST2 in chronic rhinosinusitis with nasal polyps.
abstract: OBJECTIVE
  Interleukin (IL)-33 is a novel member of the IL-1 cytokine family and a ligand for the orphan IL-1 family receptor ST2. IL-33 induces T helper 2-type inflammatory responses and is considered to play a crucial role in allergic inflammatory reactions such as asthma and atopic dermatitis. However, the role of IL-33 and its receptor ST2 in chronic rhinosinusitis remains unclear.
  
  
  METHODS
  In vitro study.
  
  
  METHODS
  The expression patterns of IL-33 and ST2 at both mRNA and protein levels in nasal polyps from eosinophilic chronic rhinosinusitis (ECRS) patients (n = 10) and non-ECRS patients (n = 13), as well as in seemingly normal mucosa of the uncinate processes in patients without sinusitis (control; n = 5), were compared using immunohistochemical staining, enzyme-linked immunosorbent assay, and real-time polymerase chain reactions.
  
  
  RESULTS
  ST2-positive cells in the inflammatory cells in the subepithelial layer were significantly higher in the ECRS group than other groups. The expression of ST2 mRNA in polyps of the ECRS group was significantly increased compared with controls. Many ST2-positive eosinophils were observed in the mucosa of ECRS but not in the mucosa of non-ECRS patients. The expression level of IL-33 mRNA was not significantly different among the three groups.
  
  
  CONCLUSIONS
  The current study suggests that IL-33 and its receptor ST2 may play important roles in the pathogenesis of chronic rhinosinusitis, especially in ECRS, through the increased expression of ST2 in eosinophils.
  
  
  METHODS
  N/A.
authors.affiliation: Department of Otolaryngology, Faculty of Medicine, The University of Tokyo, Bunkyo-ku.
authors.forename: Shintaro
authors.initials: S
authors.lastname: Baba
authors.forename: Kenji
authors.initials: K
authors.lastname: Kondo
authors.forename: Kaori
authors.initials: K
authors.lastname: Kanaya
authors.forename: Keigo
authors.initials: K
authors.lastname: Suzukawa
authors.forename: Munetaka
authors.initials: M
authors.lastname: Ushio
authors.forename: Shinji
authors.initials: S
authors.lastname: Urata
authors.forename: Takahiro
authors.initials: T
authors.lastname: Asakage
authors.forename: Akinobu
authors.initials: A
authors.lastname: Kakigi
authors.forename: Maho
authors.initials: M
authors.lastname: Suzukawa
authors.forename: Ken
authors.initials: K
authors.lastname: Ohta
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Yamasoba
mesh_terms: D000328:Adult; D000368:Aged; D002908:Chronic Disease; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007150:Immunohistochemistry; D000072179:Interleukin-1 Receptor-Like 1 Protein; D000067596:Interleukin-33; D007378:Interleukins / Q000096:biosynthesis / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009297:Nasal Mucosa / Q000378:metabolism* / Q000473:pathology; D009298:Nasal Polyps / Q000150:complications / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000235:genetics*; D012220:Rhinitis / Q000150:complications / Q000235:genetics* / Q000378:metabolism; D012852:Sinusitis / Q000150:complications / Q000235:genetics* / Q000378:metabolism
chemical_list: C079241:IL1RL1 protein, human; C506536:IL33 protein, human; D000072179:Interleukin-1 Receptor-Like 1 Protein; D000067596:Interleukin-33; D007378:Interleukins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface
keywords: Cytokine; IL-33; ST2; eosinophil; expression; inflammatory cells; nasal polyp; rhinosinusitis