Abstract
Bronchial asthma, irrespective of its specific triggers (allergens, cold, physical exercise or aspirin), is by and large an inflammatory disease. High plasma levels of immunoglobulin E (IgE), if present, indicate its atopic aetiology. Activated T lymphocytes (Th2) release various cytokines which promote recruitment, activation and secretion of mast cells, eosinophils and macrophages in the airways. Activation of these cells is associated with local release of pro-inflammatory, bronchoconstrictor or cytotoxic agents such as interleukins, proteases, superoxide anion (O2 −), histamine, platelet activating factor (PAF) and a number of eicosanoids including sulphidopeptide-leukotrienes (LTC4-E4), leukotriene B4(LTB4), thromboxane A2 (TXA2), prostaglandins F2α and D2(PGF2α and PGD2). These mediators contribute to an increase in vascular permeability, oedema, migration of leukocytes to tissues, epithelial shedding, fibroblast proliferation, bronchoconstriction, hyperreactivity of bronchi, rhinorrhea, cough and wheezing. Endogenous anti-inflammatory glucocorticoids, β adrenergic tone and the bronchodilator prostaglandin E2 (PGE2) counterbalance the pro-inflammatory cascade in the airways. Nitric oxide (NO) plays an ambiguous role in inflammatory response; however, in the lung it acts in opposition to pneumotoxic lipids (PAF, LTC4-E4, TXA2), unless overproduction of NO, together with O2 − yields toxic peroxynitrite (ONOO−).
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Gryglewski, R.J. (1998). Aspirin-induced asthma and cyclooxygenases. In: Vane, J., Botting, J. (eds) Selective COX-2 Inhibitors. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4872-6_10
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DOI: https://doi.org/10.1007/978-94-011-4872-6_10
Publisher Name: Springer, Dordrecht
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