title: ICAM-1 and alpha3beta1 expression by bronchial epithelial cells and their in vitro modulation by inflammatory and anti-inflammatory mediators.
abstract: BACKGROUND
  Adhesion molecules are involved in inflammatory and repair processes of the bronchial epithelium. ICAM-1 is mainly involved in inflammatory reactions, whereas integrins, such as alpha3beta1, are mainly involved in repair processes.
  
  
  METHODS
  Using bronchial biopsies from 10 asthmatics and eight controls, we first evaluated by immunohistochemistry expression of alpha3beta1 and ICAM-1 in intact and damaged epithelium. Then, using the human pulmonary epithelial cell line WI-26 VA, we studied, by flow-cytometry, the modulation of ICAM-1 and alpha3beta1 expression, and, by ELISA, the release of fibronectin by proinflammatory cytokines, such as IL-5, and anti-inflammatory cytokines, such as IL-4, TGF-beta, and EGF.
  
  
  RESULTS
  alpha3beta1 expression was slightly higher in asthma than in controls, as well as in damaged epithelium than in undamaged epithelium. ICAM-1 expression was higher in asthma than in controls, and similarly distributed in intact or damaged epithelium. In vitro, alpha3beta1 was significantly increased by TGF-beta, EGF, and IL-4, and significantly decreased by IL-5. Fibronectin release was significantly increased by TGF-beta and IL-4, unchanged by EGF, and slightly but significantly decreased by IL-5. ICAM-1 expression was significantly decreased by TGF-beta and IL-4, unchanged by EGF, and significantly increased by IL-5.
  
  
  CONCLUSIONS
  These differences in adhesion molecule expression and fibronectin release may be important in epithelial cell inflammation and repair.
authors.affiliation: Istituto di Fisiopatologia Respiratoria, CNR, Palermo, Italy.
authors.forename: A M
authors.initials: AM
authors.lastname: Vignola
authors.forename: G
authors.initials: G
authors.lastname: Bonsignore
authors.forename: L
authors.initials: L
authors.lastname: Siena
authors.forename: M
authors.initials: M
authors.lastname: Melis
authors.forename: G
authors.initials: G
authors.lastname: Chiappara
authors.forename: R
authors.initials: R
authors.lastname: Gagliardo
authors.forename: J
authors.initials: J
authors.lastname: Bousquet
authors.forename: G
authors.initials: G
authors.lastname: Bonsignore
authors.forename: A M
authors.initials: AM
authors.lastname: Merendino
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001249:Asthma / Q000276:immunology* / Q000378:metabolism; D001706:Biopsy; D001980:Bronchi / Q000166:cytology / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D002460:Cell Line; D016207:Cytokines / Q000494:pharmacology*; D004797:Enzyme-Linked Immunosorbent Assay; D004815:Epidermal Growth Factor / Q000494:pharmacology; D004847:Epithelial Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D005353:Fibronectins / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D007249:Inflammation; D039201:Integrin alpha3beta1; D016023:Integrins / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D015847:Interleukin-4 / Q000494:pharmacology; D008875:Middle Aged; D020545:Respiratory Mucosa / Q000166:cytology / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016212:Transforming Growth Factor beta / Q000494:pharmacology
chemical_list: D016207:Cytokines; D005353:Fibronectins; D039201:Integrin alpha3beta1; D016023:Integrins; D016212:Transforming Growth Factor beta; D018799:Intercellular Adhesion Molecule-1; D015847:Interleukin-4; D004815:Epidermal Growth Factor