Eosinophilic esophagitis (EoE) is an emerging disease characterized by esophageal
eosinophilia (>15eos/hpf), lack of responsiveness to
acid-suppressive medication and is managed by
allergen elimination and anti-
allergy therapy. Although the pathophysiology of EoE is currently unsubstantiated, evidence implicates food and aeroallergen
hypersensitivity in genetically predisposed individuals as contributory factors. Genome-wide expression analyses have isolated a remarkably conserved gene-expression profile irrespective of age and gender, suggesting a genetic contribution. EoE has characteristics of mainly TH2 type immune responses but also some TH1
cytokines, which appear to strongly contribute to tissue
fibrosis, with esophageal epithelial cells providing a hospitable environment for this inflammatory process. Eosinophil-degranulation products appear to play a central role in tissue remodeling in EoE. This remodeling and dysregulation predisposes to
fibrosis. Mast-cell-derived molecules such as
histamine may have an effect on enteric nerves and may also act in concert with
transforming growth factor-β to interfere with esophageal musculature. Additionally, the esophageal epithelium may facilitate the inflammatory process under pathogenic contexts such as in EoE. This article aims to discuss the contributory factors in the pathophysiology of EoE.