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Regulation of Inflammatory Cell Function by Corticosteroids

Respiratory Pharmacology Group, Faculty of Medicine, Imperial College London, London, United Kingdom

Correspondence and requests for reprints should be addressed to Maria G. Belvisi, Ph.D., Respiratory Pharmacology Group, Faculty of Medicine, Imperial College London, National Heart & Lung Institute, Guy Scadding Building, Dovehouse Street, London SW3 6LY, UK. E-mail: m.belvisi{at}Imperial.ac.uk

Different inflammatory cell profiles are observed in the lungs of patients with asthma versus those with chronic obstructive pulmonary disease (COPD). In asthma, several key mediators have been implicated, including tumor necrosis factor- and interleukin (IL)-1ß, together with cytokines derived from type 2 T-helper lymphocytes, such as IL-4, IL-5, and IL-13. In fact, inhibitors of IL-4 and IL-5 show promise as therapeutic agents. In COPD, the predominant inflammatory cell types are CD8⁺ T lymphocytes, macrophages, and neutrophils. Glucocorticoids inhibit eosinophils in asthma, neutrophils in COPD and severe asthma, mast cells and basophils in asthma and COPD, and macrophages in COPD. However, it is generally assumed that neutrophils are less sensitive to glucocorticoids than are eosinophils and T cells, and that macrophages from patients with COPD are less sensitive to steroid treatment under certain circumstances. These differences in the responsiveness of activated inflammatory cells may help to explain why inhaled corticosteroid treatment has been more beneficial for patients with asthma than for patients with COPD.

Key Words: asthma • chronic obstructive pulmonary disease • inhaled corticosteroids • mechanisms

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