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The role of the epithelium in airway remodeling in asthma

The role of the epithelium in airway remodeling in asthma
The role of the epithelium in airway remodeling in asthma
The bronchial epithelium is the barrier to the external environment and plays a vital role in protection of the internal milieu of the lung. It functions within the epithelial-mesenchymal trophic unit to control the local microenvironment and help maintain tissue homeostasis. However, in asthma, chronic perturbation of these homeostatic mechanisms leads to alterations in the structure of the airways, termed remodeling. Damage to the epithelium is now recognized to play a key role in driving airway remodeling. We have postulated that epithelial susceptibility to environmental stress and injury together with impaired repair responses results in generation of signals that act on the underlying mesenchyme to propagate and amplify inflammatory and remodeling responses in the submucosa. Many types of challenges to the epithelium, including pathogens, allergens, environmental pollutants, cigarette smoke, and even mechanical forces, can elicit production of mediators by the epithelium, which can be translated into remodeling responses by the mesenchyme. Several important mediators of remodeling have been identified, most notably transforming growth factor-?, which is released from damaged/repairing epithelium or in response to inflammatory mediators, such as IL-13. The cross talk between the epithelium and the underlying mesenchyme to drive remodeling responses is considered in the context of subepithelial fibrosis and potential pathogenetic mechanisms linked to the asthma susceptibility gene, a disintegrin and metalloprotease (ADAM)33.
epithelium, transforming growth factor, fibrosis, ADAM33, angiogenesis
1546-3222
678-682
Davies, Donna E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Davies, Donna E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38

Davies, Donna E. (2009) The role of the epithelium in airway remodeling in asthma. Proceedings of the American Thoracic Society, 6 (8), 678-682. (doi:10.1513/pats.200907-067DP). (PMID:20008875)

Record type: Article

Abstract

The bronchial epithelium is the barrier to the external environment and plays a vital role in protection of the internal milieu of the lung. It functions within the epithelial-mesenchymal trophic unit to control the local microenvironment and help maintain tissue homeostasis. However, in asthma, chronic perturbation of these homeostatic mechanisms leads to alterations in the structure of the airways, termed remodeling. Damage to the epithelium is now recognized to play a key role in driving airway remodeling. We have postulated that epithelial susceptibility to environmental stress and injury together with impaired repair responses results in generation of signals that act on the underlying mesenchyme to propagate and amplify inflammatory and remodeling responses in the submucosa. Many types of challenges to the epithelium, including pathogens, allergens, environmental pollutants, cigarette smoke, and even mechanical forces, can elicit production of mediators by the epithelium, which can be translated into remodeling responses by the mesenchyme. Several important mediators of remodeling have been identified, most notably transforming growth factor-?, which is released from damaged/repairing epithelium or in response to inflammatory mediators, such as IL-13. The cross talk between the epithelium and the underlying mesenchyme to drive remodeling responses is considered in the context of subepithelial fibrosis and potential pathogenetic mechanisms linked to the asthma susceptibility gene, a disintegrin and metalloprotease (ADAM)33.

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More information

Published date: December 2009
Keywords: epithelium, transforming growth factor, fibrosis, ADAM33, angiogenesis
Organisations: Clinical & Experimental Sciences

Identifiers

Local EPrints ID: 147361
URI: http://eprints.soton.ac.uk/id/eprint/147361
ISSN: 1546-3222
PURE UUID: 62ad1669-f121-4b54-a31b-b69f91fb78ca
ORCID for Donna E. Davies: ORCID iD orcid.org/0000-0002-5117-2991

Catalogue record

Date deposited: 23 Apr 2010 15:28
Last modified: 14 Mar 2024 02:32

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