title: Adhesion molecules and their ligands in nasal polyps of aspirin-hypersensitive patients.
abstract: BACKGROUND
  Chronic inflammation with tissue eosinophilia plays a key role in the pathogenesis of asthma and nasal polyps in patients with aspirin hypersensitivity.
  
  
  OBJECTIVE
  To evaluate the expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule I (ICAM-1) and their ligands (the integrins lymphocyte function-associated antigen 1 and very late-activation antigen 4 [VLA-4]) in nasal polyps of patients with aspirin hypersensitivity compared with aspirin-tolerant individuals.
  
  
  METHODS
  Immunohistochemical studies were performed using a peroxidase method and monoclonal antibodies on 6-microm-thick cryostat sections cut from frozen polyps collected during elective surgery from 21 aspirin-sensitive and 23 aspirin-tolerant patients.
  
  
  RESULTS
  The mean +/- SD values of the semiquantitatively evaluated immunoexpression of ICAM-1, VCAM-1, and VLA-4 were significantly increased in patients with aspirin hypersensitivity compared with aspirin-tolerant patients (1.7 +/- 0.8 vs 0.9 +/- 0.8, P < .003; 1.8 +/- 0.8 vs 0.8 +/- 0.8, P < .001; and 2.2 +/- 0.7 vs 1.3 +/- 0.7, P < .001, respectively), whereas the mean +/- SD values of the expression of lymphocyte function-associated antigen 1 did not differ significantly (2.4 +/- 0.5 vs 2.2 +/- 0.9; P = .57). We found a correlation between the immunoexpression of VCAM-1 and its ligand VLA-4 in all studied tissue samples (r = 0.4; P < .02).
  
  
  CONCLUSIONS
  In nasal polyps of aspirin-hypersensitive patients, up-regulation of the adhesion molecules ICAM-1 and VCAM-1 and the integrin VLA-4 may play an important role in the development of chronic eosinophilic inflammation.
authors.affiliation: Division of Pneumonology and Allergy, Department of Internal Medicine, Medical University of Lódź, Lódź, Poland. matiska@wp.pl
authors.forename: Maciej
authors.initials: M
authors.lastname: Kupczyk
authors.forename: Izabela
authors.initials: I
authors.lastname: Kupryś
authors.forename: Marian
authors.initials: M
authors.lastname: Danilewicz
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Bocheńska-Marciniak
authors.forename: Anna
authors.initials: A
authors.lastname: Murlewska
authors.forename: Paweł
authors.initials: P
authors.lastname: Górski
authors.forename: Piotr
authors.initials: P
authors.lastname: Kuna
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects / Q000276:immunology; D001241:Aspirin / Q000009:adverse effects* / Q000276:immunology; D004342:Drug Hypersensitivity / Q000276:immunology / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D039041:Integrin alpha4beta1 / Q000096:biosynthesis* / Q000276:immunology; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis* / Q000276:immunology; D016169:Lymphocyte Function-Associated Antigen-1 / Q000096:biosynthesis* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000276:immunology / Q000378:metabolism* / Q000601:surgery; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis* / Q000276:immunology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D039041:Integrin alpha4beta1; D016169:Lymphocyte Function-Associated Antigen-1; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D001241:Aspirin