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Journal of AllergyVolume 2011 2011, Article ID 257017, 7 pages

Review Article

Inflammation and Infection Research Centre, School of Medial Sciences, University of New South Wales, Sydney, NSW 2052, Australia

Centre for Asthma and Respiratory Disease, School of Biomedical Sciences, University of Newcastle and Hunter Medical Research Institute, Callaghan, NSW 2300, Australia

Received 9 May 2011; Accepted 26 August 2011

Academic Editor: Teal S. Hallstrand

Copyright © 2011 Rakesh K. Kumar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The pathogenesis of allergic asthma in childhood remains poorly understood. Environmental factors which appear to contribute to allergic sensitisation, with development of a Th2-biased immunological response in genetically predisposed individuals, include wheezing lower respiratory viral infections in early life and exposure to airborne environmental pollutants. These may activate pattern recognition receptors and-or cause oxidant injury to airway epithelial cells AECs. In turn, this may promote Th2 polarisation via a “final common pathway” involving interaction between AEC, dendritic cells, and CD4+ T lymphocytes. Potentially important cytokines produced by AEC include thymic stromal lymphopoietin and interleukin-25. Their role is supported by in vitro studies using human AEC, as well as by experiments in animal models. To date, however, few investigations have employed models of the induction phase of childhood asthma. Further research may help to identify interventions that could reduce the risk of allergic asthma.

Author: Rakesh K. Kumar, Jessica S. Siegle, Gerard E. Kaiko, Cristan Herbert, Joerg E. Mattes, and Paul S. Foster



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