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Molecular interactions between glucocorticoids and β2-agonists

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Treatment of Asthma: The long-acting beta-2-agonists
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Summary

Glucocorticoids and β2-agonists may regulate gene transcription in a cell- and gene-specific manner at both the transcriptional and post-transcriptional level. For this transcription factor interaction to be of importance in asthma, it must occur in a cell or cells which are key targets for steroids and which also express surface β2-receptors and respond to β2-agonist stimulation with elevation of cAMP. Many pulmonary cells express β2-receptors and these same cells express GR. Airway epithelial cells, T-lymphocytes and macrophages are target cells an which this effect may be of therapeutic relevance, particularly as all produce cytokines which may orchestrate or perpetuate the allergic inflammatory response.

Asthma is due to a chronic inflammation of the airways and glucocorticoids are the most effective therapy currently available for the control of asthmatic inflammation. Indeed, inhaled steroids have now become the mainstay of chronic asthma therapy. Whereas β-agonists are most effective in treating the airways constriction associated with the onset of asthma symptoms and are often the only drug prescribed for the treatment of mild asthmatics although even at this stage of the disease there may well be ongoing, possibly irreversible, inflammatory changes in the airway [1]. β-Adrenoreceptor agonists and glucocorticoids are the two most effective treatments for asthma and are often used in combination. In this chapter we summarise the interactions between these drugs at a biochemical and molecular level and discuss the possible consequences for asthma therapy.

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Adcock, I.M., Stevens, D.A. (1998). Molecular interactions between glucocorticoids and β2-agonists. In: Kummer, F. (eds) Treatment of Asthma: The long-acting beta-2-agonists. Springer, Vienna. https://doi.org/10.1007/978-3-7091-7513-2_2

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  • DOI: https://doi.org/10.1007/978-3-7091-7513-2_2

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