The University of Southampton
University of Southampton Institutional Repository

Has the time come to rethink the pathogenesis of asthma?

Has the time come to rethink the pathogenesis of asthma?
Has the time come to rethink the pathogenesis of asthma?
Purpose of review: To explore new ground in asthma pathogenesis. Asthma is an inflammatory disorder of the airways that has strong association with allergy as characterized by a Th2-type T cell response. However, ranges of approaches that have targeted this immunological component have so far been disappointing. Most asthma therapy still relies on bronchodilators and corticosteroids rather than treating underlying disease mechanisms.

Recent findings: In this review, a case is made that asthma has its primary origin in the airways that involves defective behaviour of the epithelium in relation to environmental exposures. These include defects in barrier function and an impaired innate immunity to provide the substrate upon which allergic sensitization can occur. Once the airways are sensitized repeated allergen exposure leads to disease persistence. Such mechanisms could explain airway wall remodelling and the susceptibility of the asthmatic lung to exacerbations provoked by viruses, air pollution, certain drugs, and biologically active allergens.

Summary: Activation of the epithelial-mesenchymal trophic unit could be responsible for the emergence of different asthma phenotypes and direct a more targeted approach to treatment. There is also the possibility of developing treatments that increase the lung's resistance to the inhaled environment rather than focusing on the suppression of inflammation once established.
1528-4050
48-453
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Holgate, Stephen T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc

Holgate, Stephen T. (2010) Has the time come to rethink the pathogenesis of asthma? Current Opinion in Allergy and Clinical Immunology, 10 (1), 48-453. (doi:10.1097/ACI.0b013e3283347be5). (PMID:19915457)

Record type: Article

Abstract

Purpose of review: To explore new ground in asthma pathogenesis. Asthma is an inflammatory disorder of the airways that has strong association with allergy as characterized by a Th2-type T cell response. However, ranges of approaches that have targeted this immunological component have so far been disappointing. Most asthma therapy still relies on bronchodilators and corticosteroids rather than treating underlying disease mechanisms.

Recent findings: In this review, a case is made that asthma has its primary origin in the airways that involves defective behaviour of the epithelium in relation to environmental exposures. These include defects in barrier function and an impaired innate immunity to provide the substrate upon which allergic sensitization can occur. Once the airways are sensitized repeated allergen exposure leads to disease persistence. Such mechanisms could explain airway wall remodelling and the susceptibility of the asthmatic lung to exacerbations provoked by viruses, air pollution, certain drugs, and biologically active allergens.

Summary: Activation of the epithelial-mesenchymal trophic unit could be responsible for the emergence of different asthma phenotypes and direct a more targeted approach to treatment. There is also the possibility of developing treatments that increase the lung's resistance to the inhaled environment rather than focusing on the suppression of inflammation once established.

This record has no associated files available for download.

More information

Published date: February 2010
Organisations: Clinical & Experimental Sciences

Identifiers

Local EPrints ID: 195243
URI: http://eprints.soton.ac.uk/id/eprint/195243
ISSN: 1528-4050
PURE UUID: 774dedcb-6bba-4b0b-83f3-c00b0dbe9dcf

Catalogue record

Date deposited: 17 Aug 2011 14:45
Last modified: 14 Mar 2024 04:04

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.

×