Gershwin Laurel J
Department of Pathology, Microbiology, and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA.
Curr Allergy Asthma Rep. 2007 Sep;7(5):357-62. doi: 10.1007/s11882-007-0054-7.
When allergen is inhaled it comes into contact with the epithelium of the respiratory tract. This contact triggers multiple events that can ultimately stimulate development of allergic asthma. Some allergens, like house dust mite, contain active proteolytic enzymes that break down tight epithelial cell junctions. Others act to enhance inflammation by stimulating epithelial cells to make proinflammatory cytokines and chemokines. Alterations in airways include mucous cell metaplasia and eosinophil recruitment. In this review, cell culture experiments as well as several animal models and human patient data are utilized to examine the mechanisms by which allergens alter the normal epithelial homeostasis. Environmental pollutants, such as ozone and environmental tobacco smoke, enhance allergen-mediated effects on epithelium.
当过敏原被吸入时，它会与呼吸道上皮接触。这种接触引发多种事件，最终可刺激过敏性哮喘的发展。一些过敏原，如屋尘螨，含有活性蛋白水解酶，可破坏紧密的上皮细胞连接。其他过敏原则通过刺激上皮细胞产生促炎细胞因子和趋化因子来增强炎症。气道的改变包括黏液细胞化生和嗜酸性粒细胞募集。在本综述中，利用细胞培养实验以及几种动物模型和人类患者数据来研究过敏原改变正常上皮内环境稳定的机制。环境污染物，如臭氧和环境烟草烟雾，会增强过敏原对上皮的介导作用。
