The University of Southampton
University of Southampton Institutional Repository

The airway epithelium is central to the pathogenesis of asthma.

The airway epithelium is central to the pathogenesis of asthma.
The airway epithelium is central to the pathogenesis of asthma.
Asthma is an inflammatory disorder principally involving the conducting airways and characterised by infiltration of the airway wall with a range of inflammatory cells driven in large part by activation of Th2-type lymphocytes, mast cells and eosinophils.
However a key component of asthma is the structural change that involves all of the elements of the airway wall. Here evidence is presented to suggest that the airway epithelium in asthma is fundamentally abnormal with increased susceptibility to environmental injury and impaired repair associated with activation of the epithelial-mesenchymal trophic unit (EMTU).
In addition to adopting an activated phenotype, the barrier function of the epithelium is impaired through defective tight junction formation thereby facilitating penetration of potentially toxic or damaging environmental insults. Activated and repairing epithelial cells generate a range of growth factors that are involved in the early life origins of this disease as well as its progression in the form of mucous metaplasia and airway wall remodeling.
By placing the epithelium at the forefront of asthma pathogenesis, different approaches to treatment can be devised focused more on protecting vulnerable airways against environmental injury rather than focusing on suppressing airway inflammation or manipulating the immune response.
airway remodeling, asthma, disease-susceptible genes, epithelial mesenchymal trophic unit (EMTU), thymic stromal lymphopoietin (TSLP)
1323-8930
1-10
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc

Holgate, Stephen T. (2008) The airway epithelium is central to the pathogenesis of asthma. Allergology International, 57 (1), 1-10. (doi:10.2332/allergolint.r-07-154).

Record type: Article

Abstract

Asthma is an inflammatory disorder principally involving the conducting airways and characterised by infiltration of the airway wall with a range of inflammatory cells driven in large part by activation of Th2-type lymphocytes, mast cells and eosinophils.
However a key component of asthma is the structural change that involves all of the elements of the airway wall. Here evidence is presented to suggest that the airway epithelium in asthma is fundamentally abnormal with increased susceptibility to environmental injury and impaired repair associated with activation of the epithelial-mesenchymal trophic unit (EMTU).
In addition to adopting an activated phenotype, the barrier function of the epithelium is impaired through defective tight junction formation thereby facilitating penetration of potentially toxic or damaging environmental insults. Activated and repairing epithelial cells generate a range of growth factors that are involved in the early life origins of this disease as well as its progression in the form of mucous metaplasia and airway wall remodeling.
By placing the epithelium at the forefront of asthma pathogenesis, different approaches to treatment can be devised focused more on protecting vulnerable airways against environmental injury rather than focusing on suppressing airway inflammation or manipulating the immune response.

This record has no associated files available for download.

More information

Published date: 2008
Related URLs:
Keywords: airway remodeling, asthma, disease-susceptible genes, epithelial mesenchymal trophic unit (EMTU), thymic stromal lymphopoietin (TSLP)

Identifiers

Local EPrints ID: 70833
URI: http://eprints.soton.ac.uk/id/eprint/70833
ISSN: 1323-8930
PURE UUID: 096fb6ce-5696-43a8-8e89-7a9d9c743c31

Catalogue record

Date deposited: 09 Mar 2010
Last modified: 13 Mar 2024 20:09

Export record

Altmetrics

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×