Pathogenesis of aspirin-exacerbated respiratory disease

被引：0
|
作者：
Donald D. Stevenson
Bruce L. Zuraw
机构：
[1] Scripps Clinic and The Scripps Research Institute,Allergy and Immunology Division
[2] The Scripps Clinic and Research Institute,Department of Experimental and Molecular Medicine
来源：
Clinical Reviews in Allergy & Immunology | 2003年 / 24卷
关键词：
Aspirin-exacerbated respiratory disease (AERD); leukotrienes (LTs); leukotriene E; (LTE; ); leukotriene A; (LTA; ); Cysteinyl leukotriene receptors (cysLTR); prostaglandin E; (PGE; ); prostaglandin G; (PGD; ); arachidonic acid (AA);
D O I：
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学科分类号：
摘要：
The underlying respiratory disease is activated by unknown mechanism and results in an intense infiltration of mast cells and eosinophils into the entire respiratory mucosa. These cells synthesize leukotrienes (LTs) at a very high rate and mast cells also release histamine and tryptase and synthesize PGD2 a vasodilator and bronchoconstrictor. Furthermore, AERD patients under synthesize from arachidonic acid (AA) a peculiar product called lipoxins, which opposes inflammation generated by leukotrienes. Finally, cysLT1 receptors are over expressed and highly responsive to LTE4, further augmenting the underlying inflammatory disease.
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页码：169 / 187
页数：18
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