title: Increased expression of IL-19 in the epithelium of patients with chronic rhinosinusitis and nasal polyps.
abstract: BACKGROUND
  Chronic rhinosinusitis (CRS) is an inflammation of the nose and of the paranasal sinuses. The involvement of the respiratory epithelium in the mechanisms of CRS is poorly understood.
  
  
  OBJECTIVE
  Among proteins expressed by nasal epithelial cells in CRS, IL-19 may have key functions. We here aimed to determine the expression and regulation of IL-19.
  
  
  METHODS
  Nasal biopsies from normal subjects (n = 12), subjects with CRS but without nasal polyps (NP) (CRSsNP, n = 12) and with CRS with NP (CRSwNP, n = 15) were collected. Human Asthma Gene Array and real-time PCR were used to evaluate gene expression, western blot analysis and immunohistochemistry for protein expression. Results for IL-19 were confirmed by real-time PCR. The constitutive and stimulated (LPS, TGF β) expression of IL-19 and cell proliferation were evaluated in a nasal epithelial cell line (RPMI 2650).
  
  
  RESULTS
  Human Asthma Gene Array showed an increased IL-19 gene expression in NP from patients with CRS in comparison with normal subjects. Real-time PCR confirmed the IL-19 mRNA up-regulation in patients with CRSwNP and showed an up-regulation of IL-19, at lower extent, in patients with chronic rhinosinusitis without nasal polyps (CRSsNP) in comparison with normal subjects. Western blot analysis confirmed that IL-19 is increased also at protein level in patients with CRSwNP in comparison with normal subjects. In NP, IL-19 is highly expressed in the metaplastic nasal epithelium when compared to normal or hyperplastic epithelium. LPS stimulation increased IL-19 expression, and recombinant IL-19 increased cell proliferation in nasal epithelial cells.
  
  
  CONCLUSIONS
  IL-19 is overexpressed in the epithelium in CRSwNP and increases epithelial cell proliferation.
authors.affiliation: Institute of Biomedicine and Molecular Immunology (IBIM), National Research Council (CNR), Palermo, Italy. pace@ibim.cnr.it
authors.forename: E
authors.initials: E
authors.lastname: Pace
authors.forename: V
authors.initials: V
authors.lastname: Scafidi
authors.forename: D
authors.initials: D
authors.lastname: Di Bona
authors.forename: L
authors.initials: L
authors.lastname: Siena
authors.forename: G
authors.initials: G
authors.lastname: Chiappara
authors.forename: M
authors.initials: M
authors.lastname: Ferraro
authors.forename: S
authors.initials: S
authors.lastname: La Grutta
authors.forename: S
authors.initials: S
authors.lastname: Gallina
authors.forename: R
authors.initials: R
authors.lastname: Speciale
authors.forename: A
authors.initials: A
authors.lastname: Ballacchino
authors.forename: C
authors.initials: C
authors.lastname: Bachert
authors.forename: J
authors.initials: J
authors.lastname: Bousquet
authors.forename: M
authors.initials: M
authors.lastname: Gjomarkaj
mesh_terms: D000293:Adolescent; D000328:Adult; D002908:Chronic Disease; D004847:Epithelial Cells / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D020869:Gene Expression Profiling; D006801:Humans; D007378:Interleukins / Q000235:genetics / Q000378:metabolism*; D019394:Ki-67 Antigen / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009297:Nasal Mucosa / Q000276:immunology* / Q000378:metabolism; D009298:Nasal Polyps / Q000235:genetics / Q000276:immunology*; D012333:RNA, Messenger / Q000378:metabolism; D012220:Rhinitis / Q000235:genetics / Q000276:immunology*; D012852:Sinusitis / Q000235:genetics / Q000276:immunology*; D055815:Young Adult
chemical_list: C421250:IL19 protein, human; D007378:Interleukins; D019394:Ki-67 Antigen; D012333:RNA, Messenger