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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Mori, A. et al. (1996). Enhanced Production and Gene Expression of IL-5 in Bronchial Asthma. In: Sehon, A., HayGlass, K.T., Kraft, D. (eds) New Horizons in Allergy Immunotherapy. Advances in Experimental Medicine and Biology, vol 409. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5855-2_64
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DOI: https://doi.org/10.1007/978-1-4615-5855-2_64
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