title: Functional and phenotypic characteristics of bronchial epithelial cells obtained by brushing from asthmatic and normal subjects.
abstract: Bronchial epithelial cells may be involved in the pathogenesis of asthma releasing several inflammatory mediators such as interleukins and lipoxygenase products. In this study we evaluated the spontaneous and A23128-induced release of 15-HETE, PGE2 and fibronectin as well as the spontaneous expression of HLA-DR and ICAM-1 molecules by bronchial epithelial cells obtained by bronchial brushing from 35 asthmatic and 27 normal subjects. The release of fibronectin and 15-HETE was studied using the EIA and RIA techniques. The expression of HLA-DR and ICAM-1 molecules was studied using the APAAP and the immunofluorescence methods. Bronchial epithelial cells from asthmatics released higher amounts of 15-HETE and fibronectin both spontaneously (p < 0.002, p < 0.05, respectively) or after stimulation with calcium ionophore compared with normals. On the other hand, PGE2 release was significantly higher only after stimulation with calcium ionophore (p < 0.002). The spontaneous expression of HLA-DR and ICAM-1 (p < 0.001) was significantly higher on epithelial cells from asthmatics than in normal subjects. Finally, the severity of asthma significantly correlated with the release of 15-HETE (p < 0.02) and the expression of HLA-DR and ICAM-1 respectively (p < 0.001 and p < 0.002, respectively). This study indicates that bronchial epithelial cells are in an activated state in asthma and that the degree of activation is correlated to the severity of the disease.
authors.affiliation: Service des Maladies Respiratoires, Hôpital Arnauld de Villeneuve, Montpellier, France.
authors.forename: A M
authors.initials: AM
authors.lastname: Vignola
authors.forename: P
authors.initials: P
authors.lastname: Chanez
authors.forename: A M
authors.initials: AM
authors.lastname: Campbell
authors.forename: J
authors.initials: J
authors.lastname: Bousquet
authors.forename: F B
authors.initials: FB
authors.lastname: Michel
authors.forename: P
authors.initials: P
authors.lastname: Godard
mesh_terms: D000328:Adult; D000469:Alkaline Phosphatase; D001249:Asthma / Q000276:immunology / Q000378:metabolism*; D001980:Bronchi / Q000276:immunology / Q000378:metabolism*; D000001:Calcimycin / Q000494:pharmacology; D015815:Cell Adhesion Molecules / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004848:Epithelium / Q000276:immunology / Q000378:metabolism; D005353:Fibronectins / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D006893:Hydroxyeicosatetraenoic Acids / Q000378:metabolism; D007124:Immunoenzyme Techniques; D018799:Intercellular Adhesion Molecule-1
chemical_list: D015815:Cell Adhesion Molecules; D005353:Fibronectins; D006684:HLA-DR Antigens; D006893:Hydroxyeicosatetraenoic Acids; D018799:Intercellular Adhesion Molecule-1; D000001:Calcimycin; C025984:15-hydroxy-5,8,11,13-eicosatetraenoic acid; D000469:Alkaline Phosphatase; D015232:Dinoprostone