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Epithelial–mesenchymal transition in the pathophysiology of airway remodelling in asthma

Hackett, Tillie-Louise

Current Opinion in Allergy and Clinical Immunology: February 2012 - Volume 12 - Issue 1 - p 53–59
doi: 10.1097/ACI.0b013e32834ec6eb
MECHANISMS OF ALLERGY AND ADULT ASTHMA: Edited by Stephen T. Holgate and J. Andrew Grant

Purpose of review We currently understand little about the mechanisms that lead to airway remodeling in asthma. The origin of the mesenchymal cells that contribute to fibrosis of the airway is poorly understood. However, emerging evidence suggests that the airway epithelium could contribute to airway remodeling through the process of epithelial–mesenchymal transition (EMT) following environmental challenge. In this review, we will discuss the mechanistic features of EMT and highlight recent descriptions of EMT in the airway to further define the role of the airway epithelium in the pathogenesis of asthma.

Recent findings Growth factors, inflammatory mediators, and matricellular proteins expressed following exposure to environmental insults are known to induce downregulation of epithelial cell–cell adhesions and promote mesenchymal gene expression programs both in vitro and in vivo. These results demonstrate that the plastic and dynamic airway epithelium may contribute to airway remodeling via EMT in asthma.

Summary It is becoming increasingly clear that the airway epithelium orchestrates inflammatory and remodeling responses of the airway. Understanding the regulatory mechanisms involved in epithelial plasticity will be crucial to determine effective therapies to halt the progression of airway remodeling in asthma.

aUBC James Hogg Research Centre, Institute for Heart and Lung Health, St Paul's Hospital

bDepartment of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada

Correspondence to Dr Tillie-Louise Hackett, UBC James Hogg Research Centre, St Paul's Hospital, 1081 Burrard Street, Rm 165, Vancouver, BC V6Z 1Y6, Canada. Tel: +1 604 806 8346; fax: +1 604 806 8351; e-mail:

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