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2 - Glucocorticosteroids

from Part I - Asthma and COPD

Published online by Cambridge University Press:  15 August 2009

Peter J. Barnes
Affiliation:
Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, UK
Domenico Spina
Affiliation:
King's College London
Clive P. Page
Affiliation:
King's College London
William J. Metzger
Affiliation:
National Jewish Medical and Research Centre, Denver
Brian J. O'Connor
Affiliation:
King's College London
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Summary

Introduction

Corticosteroids are the most effective therapy currently available for asthma and improvement with corticosteroids is one of the hallmarks of asthma. By contrast, corticosteroids have little or no place in the management of COPD. Inhaled corticosteroids have revolutionized asthma treatment and have become the mainstay of therapy for patients with chronic disease. There is now a much better understanding of the molecular mechanisms whereby corticosteroids suppress inflammation in asthma and this has led to changes in the way corticosteroids are used and may point the way to the development of more specific therapies in the future. This chapter discusses current understanding of the mechanism of action of corticosteroids and how corticosteroids are used in the management of asthma. The lack of benefit of corticosteroids in COPD is also discussed.

Molecular mechanisms

Corticosteroids are highly effective anti-inflammatory therapy in asthma and the molecular mechanisms involved in suppression of airway inflammation in asthma are now better understood. Corticosteroids are effective in asthma because they block many of the inflammatory pathways that are abnormally activated in asthma and they have a wide spectrum of anti-inflammatory actions.

Glucocorticoid receptors

Corticosteroids bind to a single class of glucocorticoid receptors (GR) which are localized to the cytoplasm of target cells. Corticosteroids bind at the C-terminal end of the receptor, whereas the N-terminal end of the receptor is involved in regulating gene transcription.

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Publisher: Cambridge University Press
Print publication year: 2003

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