An etiological role for aeroallergens and eosinophils in experimental esophagitis
An etiological role for aeroallergens and eosinophils in experimental esophagitis
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DOI：
10.1172/jci10224
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发表时间：
2001-01-01
影响因子：
15.9
通讯作者：
Rothenberg, ME
中科院分区：
文献类型：
--
作者：
Mishra, A;Hogan, SP;Rothenberg, ME
在胃食管反流和过敏性胃肠炎等多种疾病中均可观察到嗜酸性粒细胞浸润食管，但其过程在很大程度上尚不清楚。我们现在报告一个原始模型的实验性食管炎由暴露于呼吸道过敏原引起的小鼠。过敏原挑战小鼠出现显著水平的食管嗜酸性粒细胞、游离嗜酸性粒细胞颗粒和上皮细胞增生，这些特征与人类疾病相似。有趣的是，小鼠暴露于口腔或胃内过敏原并不会促进嗜酸性粒细胞性食管炎，这表明食管的超敏反应与肺部炎症的同时发生。此外，在缺乏eotaxin的情况下，嗜酸性粒细胞募集被减弱，而在缺乏IL-5的情况下，嗜酸性粒细胞积累和上皮增生被消除。这些结果建立了肺部和食道过敏性超敏反应之间的病理生理学联系，并证明了吸入过敏原和嗜酸性粒细胞在胃肠道炎症中的病因学作用。
Eosinophil infiltration into the esophagus is observed in diverse diseases including gastroesophageal reflux and allergic gastroenteritis, but the processes involved are largely unknown. We now report an original model of experimental esophagitis induced by exposure of mice to respiratory allergen. Allergen-challenged mice develop marked levels of esophageal eosinophils, free eosinophil granules, and epithelial cell hyperplasia, features that mimic the human disorders. Interestingly, exposure of mice to oral or intragastric allergen does not promote eosinophilic esophagitis, indicating that hypersensitivity in the esophagus occurs with simultaneous development of pulmonary inflammation. Furthermore, in the absence of eotaxin, eosinophil recruitment is attenuated, whereas in the absence of IL-5, eosinophil accumulation and epithelial hyperplasia are ablated. These results establish a pathophysiological connection between allergic hypersensitivity responses in the lung and esophagus and demonstrate an etiologic role for inhaled allergens and eosinophils in gastrointestinal inflammation.