Pathogenesis of allergen‐induced eosinophilic esophagitis is independent of interleukin (IL)‐13

Several studies have shown that interleukin (IL)‐13 is induced in the esophageal biopsies of eosinophilic esophagitis (EoE) patients and promotes esophageal eosinophilia in mice, following an IL‐13 challenge. However, the role of IL‐13 has not been clearly investigated in allergen‐induced EoE. Accordingly, we tested the hypothesis that IL‐13 is required in allergen‐induced EoE. Mice deficient in IL‐13, STAT (signal transducer and activator of transcription)6 and both IL‐4/IL‐13 genes with their respective controls were challenged with Aspergillus extract, and IL‐5 gene deficient with their control were challenged with recombinant IL‐13, intranasally. The lung and esophageal eosinophils, mast cells and collagen accumulation were examined. Herein, we report that intranasal delivery of IL‐13 promotes IL‐5‐dependent esophageal eosinophilia. However, allergen‐induced EoE is not impaired in the IL‐13 gene‐deficient mice. In addition, wild‐type and IL‐13 gene‐deficient mice demonstrated a comparable level of mast cells and collagen accumulation in the esophagus, following allergen‐induced experimental EoE. Similarly, we found that esophageal eosinophilia in IL‐4/IL‐13 double gene‐deficient and STAT6 gene‐deficient mice were also not reduced following allergen‐induced experimental EoE. In contrast, lung eosinophilia was significantly reduced in mice deficient in IL‐13, both IL‐4/IL‐13 and STAT6 genes following allergen challenge. In conclusion, our data establish that allergen‐induced EoE pathogenesis is independent of IL‐13, whereas IL‐13 is required for allergen‐induced lung eosinophilia.