title: Downregulation of polymeric immunoglobulin receptor and secretory IgA antibodies in eosinophilic upper airway diseases.
abstract: BACKGROUND
  Immunoglobulin (Ig) A represents a first-line defence mechanism in the airways, but little is known regarding its implication in upper airway disorders. This study aimed to address the hypothesis that polymeric Ig receptor (pIgR)-mediated secretory IgA immunity could be impaired in chronic upper airway diseases.
  
  
  METHODS
  Nasal and ethmoidal biopsies, as well as nasal secretions, were collected from patients with chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) or without nasal polyps (CRSsNP), allergic rhinitis (AR) and controls, and assayed for IgA1/IgA2 synthesis, pIgR expression, production of secretory component (SC), IgA and relevant IgA antibodies, and correlated with local eosinophils and inflammatory features (IL-12, IL-13 and ECP).
  
  
  RESULTS
  pIgR expression was decreased in the ethmoidal mucosa in patients with CRSwNP (P = 0.003) and in AR (P = 0.006). This pIgR defect was associated with reduced levels of SC (P = 0.007) and IgA antibodies to Staphylococcus aureus enterotoxin B (SAEB) (P = 0.003) in nasal secretions from patients with CRSwNP, and with increased IgA deposition in subepithelial areas. pIgR downregulation was selectively observed in patients with tissue eosinophilia, whilst no clear relation to smoking history was observed.
  
  
  CONCLUSIONS
  Epithelial pIgR expression is decreased in patients with CRSwNP and AR and results in decreased SC and IgA antibodies to certain bacterial antigens (SAEB) in nasal secretions of patients with CRSwNP in parallel to subepithelial accumulation of IgA. This defect in mucosal immunity is associated with eosinophilic, Th2-related inflammation.
authors.affiliation: Institut de Recherche Expérimentale et Clinique (IREC), Pole de Pneumologie, ORL & Dermatologie, Université catholique de Louvain (UCL), Brussels, Belgium; Service d'ORL, Cliniques Universitaires St-Luc, Brussels, Belgium.
authors.forename: C
authors.initials: C
authors.lastname: Hupin
authors.forename: P
authors.initials: P
authors.lastname: Rombaux
authors.forename: H
authors.initials: H
authors.lastname: Bowen
authors.forename: H
authors.initials: H
authors.lastname: Gould
authors.forename: M
authors.initials: M
authors.lastname: Lecocq
authors.forename: C
authors.initials: C
authors.lastname: Pilette
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000918:Antibody Specificity / Q000276:immunology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D015536:Down-Regulation; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism; D005260:Female; D006801:Humans; D007071:Immunoglobulin A, Secretory / Q000276:immunology* / Q000378:metabolism; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009297:Nasal Mucosa / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009298:Nasal Polyps / Q000150:complications; D019056:Receptors, Polymeric Immunoglobulin / Q000378:metabolism*; D012220:Rhinitis / Q000150:complications / Q000276:immunology* / Q000378:metabolism*; D065631:Rhinitis, Allergic; D012221:Rhinitis, Allergic, Perennial / Q000276:immunology* / Q000378:metabolism*; D012307:Risk Factors; D012635:Secretory Component / Q000276:immunology / Q000378:metabolism; D012852:Sinusitis / Q000150:complications / Q000276:immunology* / Q000378:metabolism; D055815:Young Adult
chemical_list: D016207:Cytokines; D007071:Immunoglobulin A, Secretory; D019056:Receptors, Polymeric Immunoglobulin; D012635:Secretory Component
keywords: eosinophils; epithelium; rhinitis; sinusitis