Suppr超能文献

二氧化氮可改变气管黏膜中的过敏性炎症。

Nitrogen dioxide modifies allergic inflammation in tracheal mucosa.

作者信息

Ohashi Y, Nakai Y, Okamoto H, Sugiura Y, Ohno Y, Hashimoto M, Uozumi M

机构信息

Department of Otolaryngology, Osaka City University Medical School, Japan.

出版信息

Acta Otolaryngol Suppl. 1998;538:227-32.

PMID:9879426
Abstract

Our study was designed to investigate the possible role of nitrogen dioxide exposure in respiratory allergic disorders. Guinea pigs were treated with a combination of passive sensitization, antigen challenge and nitrogen dioxide exposure. Nitrogen dioxide accumulated eosinophils to the epithelium of the trachea. Neither passive sensitization nor antigen challenge with nitrogen dioxide exposure developed more prominent pathological changes than nitrogen dioxide exposure alone. However, antigen--antibody interaction with nitrogen dioxide exposure resulted in a disruption of epithelial cells so prominent that the basement membrane was denuded in areas. Activated eosinophils and free eosinophil-specific granules were considered to be responsible for the extreme epithelial injury. In conclusion, nitrogen dioxide exposure does not cause prominent epithelial injury by itself, but could be a trigger for hyperresponsiveness in allergic airways, and is probably involved in the pathogenesis of airway allergic disorders.

摘要

我们的研究旨在调查二氧化氮暴露在呼吸道过敏性疾病中可能发挥的作用。豚鼠接受了被动致敏、抗原激发和二氧化氮暴露的联合处理。二氧化氮使嗜酸性粒细胞积聚在气管上皮。被动致敏或抗原激发与二氧化氮暴露联合处理所产生的病理变化并不比单独二氧化氮暴露更为显著。然而,抗原 - 抗体相互作用与二氧化氮暴露导致上皮细胞的破坏非常明显,以至于基底膜在某些区域裸露。活化的嗜酸性粒细胞和游离的嗜酸性粒细胞特异性颗粒被认为是导致严重上皮损伤的原因。总之,二氧化氮暴露本身不会引起明显的上皮损伤,但可能是过敏性气道高反应性的触发因素,并且可能参与气道过敏性疾病的发病机制。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验