title: Expression of endothelial and leukocyte adhesion molecules interacellular adhesion molecule-1, E-selectin, and vascular cell adhesion molecule-1 in the bronchial mucosa in steady-state and allergen-induced asthma.
abstract: BACKGROUND
  Interactions between cell adhesion molecules and their ligands are an integral part of inflammatory processes and may have direct relevance to the pathology of asthma.
  
  
  METHODS
  Immunostaining with antibodies to cell adhesion molecules was performed on bronchial biopsy specimens from persons with intrinsic and extrinsic asthma, normal nonasthmatic control subjects, and patients with asthma after allergen challenge.
  
  
  RESULTS
  There was constitutive expression of intercellular adhesion molecule-1 (ICAM-1), E-selectin and vascular cell adhesion molecule-1 (VCAM-1) in patients with intrinsic and extrinsic asthma and in control subjects. Compared with control subjects, ICAM-1 and E-selectin staining in the submucosa was greater in the intrinsic asthmatic group for intensity (p < 0.02, p < 0.05) and extent (p < 0.01, p < 0.05) of staining, respectively. No differences were observed between patients with extrinsic asthma and normal control subjects, and VCAM-1 expression did not differ among the groups. Epithelial expression of ICAM-1 was more frequent in patients with asthma compared with normal control subjects (p < 0.05). Compared with diluent challenge, bronchial biopsy specimens obtained 24 hours after allergen challenge revealed no significant differences in intensity or extent of staining for ICAM-1, E-selectin, or VCAM-1. After allergen challenge, the intensity and extent of both VCAM-1 and ICAM-1 expression correlated significantly with the number of eosinophils (cells positive for major basic protein). Epithelial ICAM-1 expression was more frequently observed after allergen challenge than after diluent challenge (p < 0.02).
  
  
  CONCLUSIONS
  The data suggest a complex pattern of regulation for ICAM-1, E-selectin, and VCAM-1 in vivo, where they may reflect the degree of ongoing inflammation in asthma.
authors.affiliation: Department of Allergy and Clinical Immunology, National Heart and Lung Institute, London, England.
authors.forename: A M
authors.initials: AM
authors.lastname: Bentley
authors.forename: S R
authors.initials: SR
authors.lastname: Durham
authors.forename: D S
authors.initials: DS
authors.lastname: Robinson
authors.forename: G
authors.initials: G
authors.lastname: Menz
authors.forename: C
authors.initials: C
authors.lastname: Storz
authors.forename: O
authors.initials: O
authors.lastname: Cromwell
authors.forename: A B
authors.initials: AB
authors.lastname: Kay
authors.forename: A J
authors.initials: AJ
authors.lastname: Wardlaw
mesh_terms: D000328:Adult; D000485:Allergens / Q000008:administration & dosage; D001249:Asthma / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D001980:Bronchi / Q000276:immunology*; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D019040:E-Selectin; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1; D008297:Male; D008875:Middle Aged; D009092:Mucous Membrane / Q000276:immunology; D019010:Vascular Cell Adhesion Molecule-1
chemical_list: D000485:Allergens; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1