The University of Southampton
University of Southampton Institutional Repository

Bronchial epithelium as a key regulator of airway allergen sensitization and remodeling in asthma

Bronchial epithelium as a key regulator of airway allergen sensitization and remodeling in asthma
Bronchial epithelium as a key regulator of airway allergen sensitization and remodeling in asthma
Asthma is a chronic inflammatory disorder of the airways manifesting as intermittent airflow limitation, which over time may become progressive (1). Both in the allergic and nonallergic forms of the disease there is evidence of an altered local T cell response in favor of Th2 cytokine release resulting in B cell isotype switching to IgE; mast cell, eosinophil, and basophil recruitment; and activation and release of a wide range of inflammatory mediators (2). However, it has become clear that, by itself, inflammation is not able to explain many of the features characteristic of chronic asthma and that restructuring of the airway wall is also required (3). This “remodeling” response presumably accounts for the incomplete therapeutic efficacy of corticosteroids, with persistence of bronchial hyperresponsiveness (BHR), and the progressive decline in pulmonary function over time that occurs in those asthmatic individuals with more chronic and severe disease (1). Although atopy, the propensity to generate allergen-specific IgE, is one of the strongest risk factors for asthma, especially in children and young adults, only 10% of atopics develop chronic asthma and, as adults, asthma occurs in the absence of atopy, most notably in those with more severe and chronic disease. It seems plausible that, rather than IgE-mediated inflammation being the initiator of disordered airway function, the epithelium itself is abnormal and it is this that predisposes the individual with asthma toward local allergen sensitization, and the injurious effects of respiratory viruses and air pollutants (including tobacco smoke). A disordered epithelium could also provide a basis for airway remodeling in asthma.
1073-449X
S113-S117
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Lackie, Peter
4afbbe1a-22a6-4ceb-8cad-f3696dc43a7a
Wilson, Susan
21c6875d-6870-441b-ae7a-603562a646b8
Roche, William
a5135b2d-cab5-481b-887a-78611fa00bff
Davies, Donna
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Lackie, Peter
4afbbe1a-22a6-4ceb-8cad-f3696dc43a7a
Wilson, Susan
21c6875d-6870-441b-ae7a-603562a646b8
Roche, William
a5135b2d-cab5-481b-887a-78611fa00bff
Davies, Donna
7de8fdc7-3640-4e3a-aa91-d0e03f990c38

Holgate, Stephen T., Lackie, Peter, Wilson, Susan, Roche, William and Davies, Donna (2000) Bronchial epithelium as a key regulator of airway allergen sensitization and remodeling in asthma. American Journal of Respiratory and Critical Care Medicine, 162 (3), S113-S117. (doi:10.1164/ajrccm.162.supplement_2.ras-12).

Record type: Article

Abstract

Asthma is a chronic inflammatory disorder of the airways manifesting as intermittent airflow limitation, which over time may become progressive (1). Both in the allergic and nonallergic forms of the disease there is evidence of an altered local T cell response in favor of Th2 cytokine release resulting in B cell isotype switching to IgE; mast cell, eosinophil, and basophil recruitment; and activation and release of a wide range of inflammatory mediators (2). However, it has become clear that, by itself, inflammation is not able to explain many of the features characteristic of chronic asthma and that restructuring of the airway wall is also required (3). This “remodeling” response presumably accounts for the incomplete therapeutic efficacy of corticosteroids, with persistence of bronchial hyperresponsiveness (BHR), and the progressive decline in pulmonary function over time that occurs in those asthmatic individuals with more chronic and severe disease (1). Although atopy, the propensity to generate allergen-specific IgE, is one of the strongest risk factors for asthma, especially in children and young adults, only 10% of atopics develop chronic asthma and, as adults, asthma occurs in the absence of atopy, most notably in those with more severe and chronic disease. It seems plausible that, rather than IgE-mediated inflammation being the initiator of disordered airway function, the epithelium itself is abnormal and it is this that predisposes the individual with asthma toward local allergen sensitization, and the injurious effects of respiratory viruses and air pollutants (including tobacco smoke). A disordered epithelium could also provide a basis for airway remodeling in asthma.

Full text not available from this repository.

More information

Published date: 2000

Identifiers

Local EPrints ID: 27101
URI: https://eprints.soton.ac.uk/id/eprint/27101
ISSN: 1073-449X
PURE UUID: 7d2440eb-7af2-492b-8247-4c4f2d3b4233
ORCID for Peter Lackie: ORCID iD orcid.org/0000-0001-7138-3764
ORCID for Donna Davies: ORCID iD orcid.org/0000-0002-5117-2991

Catalogue record

Date deposited: 27 Apr 2006
Last modified: 20 Jul 2019 01:28

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 https://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.

×