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Editorial || FREE PAPER ||

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Author: Garry M Walsh

Published Date May 2007 Volume 2007:3(2) Pages 211 - 212
DOI: http://dx.doi.org/10.2147/TCRM.S

Garry M Walsh

Asthmatic and Allergy Inflammation Group, School of Medicine, University of Aberdeen, UK

Abstract: Asthma is now one of the most common chronic diseases in westernized countries and is characterized by reversible airway obstruction, bronchial hyperresponsiveness, and airway inflammation. Key pathological features include: infiltration of the airways by activated lymphocytes and eosinophils; damage to, and loss of, the bronchial epithelium; mast cell degranulation; mucous gland hyperplasia; and collagen deposition in the epithelial sub-basement membrane area. Presently, antiinflammatory therapy in asthma is largely reliant on corticosteroids, particularly in their inhaled form, and their use is associated with a striking reduction in the numbers of activated eosinophils, mast cells, and T cells in vivo. For the majority of patients, corticosteroids are effective at suppressing airway inflammation and the associated re-modelling of the airways that leads to progressive and irreversible loss of lung function.