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An etiological role for aeroallergens and eosinophils in experimental esophagitis
Anil Mishra, … , Eric B. Brandt, Marc E. Rothenberg
Anil Mishra, … , Eric B. Brandt, Marc E. Rothenberg
Published January 1, 2001
Citation Information: J Clin Invest. 2001;107(1):83-90. https://doi.org/10.1172/JCI10224.
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Article

An etiological role for aeroallergens and eosinophils in experimental esophagitis

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Abstract

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.

Authors

Anil Mishra, Simon P. Hogan, Eric B. Brandt, Marc E. Rothenberg

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Figure 1

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The effect of oral, intragastric, and intranasal allergen challenge on e...
The effect of oral, intragastric, and intranasal allergen challenge on eosinophil levels in the esophagus. Mice (BALB/c) were challenged with repeated inoculations of oral, intragastric and intranasal allergen. Eighteen hours after the last allergen or placebo challenge, the mice were sacrificed and eosinophil levels were evaluated in the esophagus. Data are expressed as mean ± SEM; n = 8–9 mice.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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