An etiological role for aeroallergens and eosinophils in experimental esophagitis

Eosinophil infiltration into the esophagus is observed in diverse diseases including gastroesophageal reflux and allergic gastroenteritis, but the pro cesses involved are largely unknown. We now report an original model of exp erimental esophagitis induced by exposure of mice to respiratory allergen. Allergen-challenged mice develop marked levels of esophageal eosinophils, f ree eosinophil granules, and epithelial cell hyperplasia, features that mim ic the human disorders. Interestingly, exposure of mice to oral or intragas tric allergen does not promote eosinophilic esophagitis, indicating that hy persensitivity in the esophagus occurs with simultaneous development of pul monary inflammation. Furthermore, in the absence of eotaxin, eosinophil rec ruitment is attenuated, whereas in the absence of IL-5, eosinophil accumula tion and epithelial hyperplasia are ablated. These results establish a path ophysiological connection between allergic hypersensitivity responses in th e lung and esophagus and demonstrate an etiologic role for inhaled allergen s and eosinophils in gastrointestinal inflammation.