Allergic components of eosinophilic esophagitis

Abstract

Eosinophilic esophagitis (EoE) is a disorder of increasing prevalence worldwide, causing clinical symptoms of vomiting, failure to thrive, and dysphagia and complications of esophageal remodeling with strictures and food impactions. Molecular profiling demonstrates EoE to be an eosinophil-predominant disorder with a T_H2 cytokine profile reminiscent of other allergic diseases, such as asthma, allergic rhinitis, and atopic dermatitis. Environmental antigens in the form of foods and aeroallergens induce eosinophil, basophil, mast cell, and T-cell infiltration. Pathogenesis depends on local epithelial immune activation with production of thymic stromal lymphopoietin and eotaxin-3. Complications mirror asthmatic airway pathogenesis, with increases in subepithelial collagen deposition, angiogenesis, and smooth muscle hypertrophy. The removal of instigating antigens, especially foods, causes disease resolution in more than 50% of adults and children. The prevalence of concurrent atopic disorders in patients with EoE and the need to control antigen-specific T_H2 inflammation underscore the importance of testing for allergens and treating the entire atopic subject to control the potential interplay between organ-specific allergic responses.

Keywords: Esophagitis; allergic rhinitis; allergy testing; antigens; food allergy.

Figure 1. Food and Aeroallergen Antigens in EoE

Ingested and inhaled antigens, in conjunction with acid and proteases, activate the epithelium to produce chemotactic and activating factors for innate (mast cells, basophils, iNKT, innate lymphoid cells) and adaptive (T cells) immune cells. Infiltrating cells can produce Th2 cytokines such as IL-13 and IL-4 as well as pro-fibrotic factors. Chronic inflammation initiates tissue remodeling with resultant dysphagia, food impactions, and strictures.