Tissue remodeling in eosinophilic esophagitis.

Abstract

Eosinophilic esophagitis (EoE) is a chronic inflammatory disease characterized by esophageal dysfunction and tissue eosinophilia that is often associated with food impaction and dysphagia. The disease is triggered by allergic hypersensitivity to food involving a strong type 2 immune response accompanied by tissue remodeling and, if left untreated, there can be progression to strictures thought to be due, in part, to unabated lamina propria fibrosis. The composite finding of fibrosis and stenosis is referred to as "fibrostenosis." Current pharmacologic therapies include approved topical corticosteroid formulations and a precision mAb targeting type 2 immunity, yet it is not clear whether these therapies universally reverse fibrosis. This could be due, in part, to the complexity of the underlying tissue remodeling process, involving various cells and molecular pathways that extend beyond isolated type 2 immunity and that can create a feed-forward loop. This review discusses the need for prompt diagnosis and treatment in EoE, the identification of histologic parameters and/or biomarkers of potential progression to tissue remodeling, and the current state of research into key cellular and molecular mediators that drive tissue remodeling in EoE.