Corticosteroids not only have a wide range of anti-inflammatory effects in vitro, but also cause a reduction in airways inflammation when inhaled by asthmatic patients (1,2). This evidence comes primarily from bronchial biopsy studies demonstrating that regular treatment with ICS such as beclo-methasone dipropionate (BDP), budesonide, and fluticasone propionate (FP) cause a marked reduction in the number of mast cells, T lymphocytes, and eosinophils in the epithelium and submucosa (3-8). There is also a reduction in inflammatory cell activation, as reflected by decreased concentrations of cell-derived mediators in bronchial lavage fluid (9-11).
At the cellular level, ICS suppress both acute and chronic inflammation, irrespective of the underlying cause, by inhibiting many steps in the inflammatory process (Fig. 1). The disrupted epithelium is restored and the ciliated cell/goblet cell ratio is normalized with long-term treatment (3). There is also some evidence of a reduction in the thickness of the basement membrane, leading to the suggestion that ICS may influence the process of airways remodeling in asthma (6,7). The clinical efficacy of ICS is considered to be primarily due to the reduction in airways inflammation.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.