Allergy and eosinophil-associated gastrointestinal disorders (EGID)

Abstract

Eosinophil-associated gastrointestinal disorders (EGIDs) are characterized by an inappropriate accumulation of eosinophils within the gastrointestinal tract. The underlying etiology and pathophysiology that lead to the development of EGID are far from elucidated. However, there is growing evidence to support the role of aeroallergens and food allergens in the pathogenesis of these disorders. Recent advances have highlighted the role of Th2-driven cytokines in the development of EGID, and clinical studies have verified that children and adults with EGID often have positive skin testing to food allergens. The most common form of EGID, eosinophilic esophagitis (EE), has garnered intense investigation following an increased recognition over the past decade. Recently, there have been several important studies providing insight into both the cellular mechanisms governing EE and clinical therapies directed toward the treatment of EE. In the article herein, we will review the most recent scientific advances influencing our understanding of EGID with special emphasis on the role of allergens in the pathogenesis of EGID.

Figure 1. Molecular Pathogenesis of Eosinophilic Esophagitis

EE arises from the interaction between genetic factors and environmental exposures. This interaction leads to the secretion of a complex array of cellular mediators. The expression of IL-13 and TGF-β likely contributes to the release of eotaxin-3, increased collagen production (fibrosis) and vascular activation (VCAM-1). Finally, IgE can be detected on the surface of mast cells and likely contributes to mast cell activation. This figure was adapted with the publisher's permission.