title: Enhanced soluble interleukin-5 receptor alpha expression in nasal polyposis.
abstract: BACKGROUND
  Alternative splicing of the interleukin-5 receptor alpha (IL-5Ralpha)-subunit leads to the generation of a signalling, membrane-anchored (TM) isoform, or a secreted [soluble (SOL)], antagonistic variant. Given the key role of IL-5 in eosinophil function, we investigated SOL IL-5Ralpha expression pattern in an eosinophil-associated disease such as nasal polyposis (NP).
  
  
  METHODS
  An SOL IL-5Ralpha enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction (PCR) were established and applied in serum, nasal secretion and nasal tissue of controls (n = 12), and NP patients (n = 42) with or without asthma.
  
  
  RESULTS
  Analysis of serum, nasal secretion, and nasal tissue samples revealed that SOL IL-5Ralpha protein concentrations were significantly increased in NP vs control tissue. Within the NP group, there was a significant up-regulation of SOL IL-5Ralpha in patients with systemic airway disease. These findings were confirmed at the mRNA level, using an optimized real-time reverse-transcriptase PCR procedure.
  
  
  CONCLUSIONS
  This report demonstrates SOL IL-5Ralpha transcript and protein up-regulation in NP. Soluble IL-5Ralpha differentiates nasal polyps with or without concomitant asthma. As SOL IL-5Ralpha is strongly up-regulated for disease and has antagonistic properties in vitro, our studies shed new light on the mechanisms of specific immunomodulatory therapies, such as anti-IL-5.
authors.affiliation: Department of Otorhinolaryngology, Ghent University Hospital, Belgium.
authors.forename: P
authors.initials: P
authors.lastname: Gevaert
authors.forename: C
authors.initials: C
authors.lastname: Bachert
authors.forename: G
authors.initials: G
authors.lastname: Holtappels
authors.forename: C P
authors.initials: CP
authors.lastname: Novo
authors.forename: J
authors.initials: J
authors.lastname: Van der Heyden
authors.forename: L
authors.initials: L
authors.lastname: Fransen
authors.forename: S
authors.initials: S
authors.lastname: Depraetere
authors.forename: H
authors.initials: H
authors.lastname: Walter
authors.forename: P
authors.initials: P
authors.lastname: van Cauwenberge
authors.forename: J
authors.initials: J
authors.lastname: Tavernier
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal; D001249:Asthma / Q000276:immunology; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000276:immunology; D005260:Female; D006801:Humans; D015848:Interleukin-5 / Q000097:blood / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009297:Nasal Mucosa / Q000276:immunology; D009298:Nasal Polyps / Q000276:immunology*; D012333:RNA, Messenger / Q000097:blood; D018123:Receptors, Interleukin / Q000097:blood / Q000378:metabolism*; D053649:Receptors, Interleukin-5; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D000911:Antibodies, Monoclonal; D015848:Interleukin-5; D012333:RNA, Messenger; D018123:Receptors, Interleukin; D053649:Receptors, Interleukin-5