Eosinophilic Esophagitis and Inflammatory Bowel Disease: What Are the Differences?

Int J Mol Sci. 2024 Aug 5;25(15):8534. doi: 10.3390/ijms25158534.

Abstract

Eosinophilic esophagitis (EoE) and inflammatory bowel disease (IBD) are chronic inflammatory disorders of the gastrointestinal tract, with EoE predominantly provoked by food and aeroallergens, whereas IBD is driven by a broader spectrum of immunopathological and environmental triggers. This review presents a comprehensive comparison of the pathophysiological and therapeutic strategies for EoE and IBD. We examine the current understanding of their underlying mechanisms, particularly the interplay between environmental factors and genetic susceptibility. A crucial element in both diseases is the integrity of the epithelial barrier, whose disruption plays a central role in their pathogenesis. The involvement of eosinophils, mast cells, B cells, T cells, dendritic cells, macrophages, and their associated cytokines is examined, highlighting the importance of targeting cytokine signaling pathways to modulate immune-epithelial interactions. We propose that advances in computation tools will uncover the significance of G-protein coupled receptors (GPCRs) in connecting immune and epithelial cells, leading to novel therapies for EoE and IBD.

Keywords: eosinophilic esophagitis; epithelial barrier disruption; immune-mediated epithelial damage; immune–epithelial crosstalk; inflammatory bowel disease; mucosal barrier integrity.

Publication types

  • Review

MeSH terms

  • Animals
  • Cytokines / metabolism
  • Eosinophilic Esophagitis* / etiology
  • Eosinophilic Esophagitis* / immunology
  • Eosinophilic Esophagitis* / pathology
  • Eosinophilic Esophagitis* / therapy
  • Eosinophils / immunology
  • Eosinophils / metabolism
  • Eosinophils / pathology
  • Genetic Predisposition to Disease
  • Humans
  • Inflammatory Bowel Diseases* / etiology
  • Inflammatory Bowel Diseases* / immunology
  • Inflammatory Bowel Diseases* / metabolism
  • Inflammatory Bowel Diseases* / pathology

Substances

  • Cytokines