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ASTHMA AND COPD: MECHANISM OF ACTION OF GLUCOCORTICOIDS, β2-AGONISTS AND THEIR COMBINATION
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Introduction
 
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Introduction
Introduction

Asthma and COPD are both chronic inflammatory diseases of the respiratory system, although characterised by distinct pathophysiological and clinical features. The inflammatory process in COPD differs from that in asthma for inflammatory cells, mediators, inflammatory effects and, consequently, for response to therapy.

Understanding the main distinct characteristics of inflammation in asthma and COPD is crucial to comprehend why the two diseases responses to inhaled corticosteroids (ICSs) and inhaled long-acting β2-agonists (LABAs) are so different.

Asthma is mainly characterised by airway inflammation, remodelling and smooth muscle dysfunction. Acute and chronic airway inflammation in asthma is due to the recruitment and activation of a wide range of inflammatory cells, such as eosinophils, CD4+ T lymphocytes and mast cells, and to the release of multiple mediators (mainly cytokines, interleukin (IL)-4 and 13, and chemokines), which sustain the inflammatory process.

Also COPD is characterised by an inflammatory component, besides structural changes and mucociliary dysfunction. However, inflammation in COPD is associated to an increase in different inflammatory cells (CD8+ T lymphocytes, monocytes/macrophages and neutrophils) and mediators (i.e. IL-8, tumor necrosis factor (TNF)-α, leukotriene B4) (Fig. 1).1

Figure 1: Characteristics of inflammation in COPD and asthma (GINA guidelines).2

The standard therapy for both the diseases includes the administration of LABAs and ICSs, following a specific therapeutic strategy and applying a progressive increase in therapy, which are distinctive for each disease.

In asthma, ICSs are the first-line therapy due to the fact that are specifically effective on the inflammatory process which characterises the disease. Furthermore, there is strong evidence that the addition of a LABA to a daily ICS regimen improves asthma symptoms and lung function, decreases nocturnal asthma and the use of short-acting inhaled β2-agonists, and reduces the number of exacerbations. Thus, the preferred therapy for moderate persistent asthma is regular treatment with a combination of an ICS and a LABA twice daily, and the primary therapy for severe persistent asthma includes ICS at higher doses plus a LABA.

In COPD, since the inflammatory process is not responsive to steroids, the mainstays of treatment are bronchodilators, including LABAs. The benefits related to the addition of an ICS to a LABA have been currently demonstrated only in patients with severe disease.

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