阿司匹林加重的呼吸道疾病和反应的发病机制。
Pathogenesis of aspirin-exacerbated respiratory disease and reactions.
机构信息
Brigham and Women's Hospital, Department of Medicine, Division of Rheumatology, Immunology and Allergy, Jeff and Penny Vinik Center for Allergic Disease Research, Boston, MA 02115, USA.
出版信息
Immunol Allergy Clin North Am. 2013 May;33(2):195-210. doi: 10.1016/j.iac.2012.11.006. Epub 2012 Dec 23.
Abstract
Physiologic and pharmacologic studies support the hypothesis that aspirin-exacerbated respiratory disease (AERD) involves fundamental dysregulation in the production of and end-organ responsiveness to both antiinflammatory eicosanoids (prostaglandin E2) and proinflammatory effectors (cysteinyl leukotrienes). The acquired nature of AERD implies a disturbance in a potential epigenetic control mechanism of the relevant mediator systems, which may be a result of incompletely clarified environmental factors (eg, viral or bacterial infections, inhaled pollutants).
摘要
生理和药理研究支持这样一种假说，即阿司匹林加重的呼吸道疾病（AERD）涉及到抗炎症类二十烷（前列腺素 E2）和促炎症效应物（半胱氨酰白三烯）的产生及其对终末器官的反应性的根本失调。AERD 的获得性暗示了相关介质系统的潜在表观遗传控制机制发生了紊乱，这可能是由于尚未完全阐明的环境因素（例如，病毒或细菌感染、吸入性污染物）所致。
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