Abstract
Infiltration of various inflammatory cells into the bronchial mucosa and submucosa is a prominent pathological feature of bronchial asthma.1–3 Persistent mucosal inflammation, particularly epithelial damage caused by eosinophil-derived products, is believed to contribute to the pathogenesis of bronchial hypersensitivity.4–7 Inhalation of a relevant allergen results in an early asthmatic reaction (EAR) that subsides within 1 to 2 hours. In 40–60% of patients, this early reaction is followed after 6 to 10 hours by a late asthmatic reaction (LAR), which usually subsides during the next 1 to 2 days.8 Accumulating evidence suggests that LAR is a consequence of eosinophilic inflammation in the lung induced by a T cell cytokine, interleukin 5 (IL-5).9–15
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