Apoptosis and loss of adhesion of bronchial epithelial cells in asthma

Trautmann A., Kruger K., Akdis M., Muller-Wening D., Akkaya A., Brocker E., ...More

INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, vol.138, no.2, pp.142-150, 2005 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 138 Issue: 2
  • Publication Date: 2005
  • Doi Number: 10.1159/000088436
  • Journal Indexes: Science Citation Index Expanded, Scopus
  • Page Numbers: pp.142-150


Background: Asthma is an inflammatory airway disease associated with infiltration of T cells and eosinophils, increased levels of pro-inflammatory cytokines, and shedding of bronchial epithelial cells (EC). We have recently shown that T cells and eosinophils cooperate in inducing bronchial EC apoptosis in asthma through secretion of IFN-gamma and TNF-alpha. Since EC shedding is a histologic hallmark of asthma, the intercellular junction of EC may be a target of pro-inflammatory cytokines. Methods: Bronchial EC, cultured and exposed to IFN-gamma and TNF-alpha, were studied for the expression of adhesion molecules and apoptosis. In addition, the epithelial layer of bronchial biopsies from asthma patients was evaluated for apoptosis, shedding, and expression of adhesion molecules. Results: We demonstrate that the induction of EC apoptosis is accompanied by loss of E-cadherin. In situ examination of E-cadherin in asthma revealed a reduction in its expression on EC membranes. In contrast, the in vitro and in vivo expression of beta(1)- integrins and intercellular adhesion molecule-1 (ICAM-1) increased on EC during asthmatic airway inflammation. Conclusions: Loss of cadherin-mediated intercellular adhesion and apoptosis could account for fragility and shedding of EC in asthma, especially since this occurs between columnar and basal EC. Copyright (C) 2005 S. Karger AG, Basel.