Abstract
These are revolutionary times for patients with asthma. The disease is no longer considered the consequence of just bronchospasm or hyperactive airways. Rather, even in its mildest form asthma is considered an inflammatory disease, often described as "chronic desquamating eosinophilic bronchitis."1 , 2 The respiratory epithelium appears to bear the brunt of the inflammatory attack; it is vacuolated, and ciliated cells are shed into the bronchial lumen. Eosinophils not only become more numerous in the blood, the bronchial mucosa, and the sputum, but also damage the epithelium.3 Studies using bronchoalveolar lavage and endobronchial biopsy combined with the techniques of cellular and molecular . . .

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