title: HLA-DR and ICAM-1 expression and modulation in epithelial cells from nasal polyps.
abstract: OBJECTIVE
  Through human leukocyte antigen-DR (HLA-DR) and intercellular adhesion molecule-1 (ICAM-1) expression, nasal epithelial cells could actively participate in the chronic inflammation and eosinophil infiltration observed in nasal polyps. The objective of the study was to evaluate HLA-DR and ICAM-1 expression in polyp epithelium and in a culture model of polyp epithelial cells allowing ciliated and secretory differentiation.
  
  
  METHODS
  Prospective non-randomized controlled in vitro study.
  
  
  METHODS
  The in vitro HLA-DR and ICAM-1 expression was studied under basal conditions or after exposure to interferon-gamma, transforming growth factor-beta1, lipopolysaccharide, dexamethasone, or cetirizine. HLA-DR and ICAM-1 expression was investigated in situ by immunohistochemical staining of polyps and in vitro by immunofluorescent staining of cell cultures. HLA-DR and ICAM-1 were localized in cultured cells by confocal microscopy. Cultured cells expressing HLA-DR and ICAM-1 were quantified by flow cytometry.
  
  
  RESULTS
  Both HLA-DR and ICAM-1 showed significant immunostaining of nasal polyp epithelium. In nasal polyp epithelial cell cultures, less than 5% of cells were positive for HLA-DR whereas 40% were positive for ICAM-1 at day 3. In vitro, HLA-DR was mainly located in the cytoplasm and ICAM-1 predominated on the apicolateral cytoplasmic membrane. Comparison of in situ and in vitro results showed that well-differentiated and poorly differentiated cells predominantly expressed HLA-DR and ICAM-1, respectively. Interferon-gamma significantly increased HLA-DR and ICAM-1 expression, whereas transforming growth factor-beta1 significantly decreased HLA-DR expression and lipopolysaccharide significantly increased ICAM-1 expression.
  
  
  CONCLUSIONS
  HLA-DR and ICAM-1 epithelial expression in nasal polyps in situ and in vitro and their in vitro modulation reinforce the active role of epithelial cells in chronic inflammatory diseases of the upper airways.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale, Unité U492, Faculté de Médecine, Paris XII, Créteil, France.
authors.forename: Jean-François
authors.initials: JF
authors.lastname: Papon
authors.forename: André
authors.initials: A
authors.lastname: Coste
authors.forename: Marie-Claude
authors.initials: MC
authors.lastname: Gendron
authors.forename: Catherine
authors.initials: C
authors.lastname: Cordonnier
authors.forename: Laure
authors.initials: L
authors.lastname: Wingerstmann
authors.forename: Roger
authors.initials: R
authors.lastname: Peynègre
authors.forename: Estelle
authors.initials: E
authors.lastname: Escudier
mesh_terms: D000704:Analysis of Variance; D002478:Cells, Cultured; D017332:Cetirizine / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004847:Epithelial Cells / Q000276:immunology / Q000378:metabolism*; D005434:Flow Cytometry; D006684:HLA-DR Antigens / Q000096:biosynthesis*; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis*; D007371:Interferon-gamma / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D018613:Microscopy, Confocal; D009298:Nasal Polyps / Q000276:immunology / Q000378:metabolism*; D011446:Prospective Studies; D016212:Transforming Growth Factor beta / Q000494:pharmacology
chemical_list: D006684:HLA-DR Antigens; D008070:Lipopolysaccharides; D016212:Transforming Growth Factor beta; D018799:Intercellular Adhesion Molecule-1; D003907:Dexamethasone; D007371:Interferon-gamma; D017332:Cetirizine