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.