Abstract
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.
Highlights
Eosinophilic esophagitis (EoE) is an emerging condition characterized by severe isolated eosinophilic infiltration of the esophageal mucosa (1)
A recent study on the effect of IL-13 on genes involved in epithelial differentiation concluded that IL-13 plays a large role in the up-regulation of genes such as Ki67 and down-regulation of epithelial differentiation cluster (EDC) genes such as filaggrin and involucrin, which cumulatively contribute to the eotaxin-mediated recruitment of eosinophils to the esophageal epithelium
In summary, EoE is an inflammatory disorder (Table 1) that may be initiated by a hypersensitivity reaction to aero- or food allergens, with a late-phase characterized by eosinophil recruitment and subsequent tissue damage
Summary
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. The pathophysiology of EoE is currently unsubstantiated, evidence implicates food and aeroallergen hypersensitivity in genetically predisposed individuals as contributory factors. EoE has characteristics of mainly TH2 type immune responses and 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. 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
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