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Department of
Thoracic Medicine, National Heart & Lung Institute, Imperial College
School of Medicine, Dovehouse Street, London SW3 6LY, UK
Correspondence to: Dr R Newton email: robert.newton@ic.ac.uk
Received 28 February 2000; Accepted for publication 1 March 2000
| The first 150 words of the full text of this article appear below. |
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Biological effects of glucocorticoids |
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Inflammatory diseases such as asthma and rheumatoid arthritis are
characterised at the molecular level by chronically increased expression of multiple cytokines, chemokines, kinins and their receptors, adhesion molecules, and inflammatory enzymes such as inducible nitric oxide synthase (iNOS) and the inducible cyclooxygenase (COX-2).1 At the cellular level, inflamed regions show a
substantial influx of various inflammatory cells, arterial dilation,
increased blood flow, plasma protein leakage, and oedema whilst, in the case of chronic asthma, substantial remodelling of the airways is
observed involving excessive smooth muscle proliferation. However, these parameters of inflammation are effectively reduced by treatment with glucocorticoids by both direct and indirect
mechanisms.2 3 For example, the reduced eosinophilia
following glucocorticoid treatment in asthmatic subjects arises by
direct promotion of eosinophil apoptosis and indirectly by suppressing
receptor expression and production of cytokines or growth
factors.4 These include factors such as interleukin
(IL)-3, IL-5, granulocyte-macrophage colony stimulating factor
(GM-CSF), and eotaxin
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