Ohashi Y, Nakai Y, Okamoto H, Sugiura Y, Ohno Y, Hashimoto M, Uozumi M
Department of Otolaryngology, Osaka City University Medical School, Japan.
Acta Otolaryngol Suppl. 1998;538:227-32.
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.
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。
