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Pathophysiology of Eosinophilic Esophagitis

Authors
  • O'Shea, Kelly M.1
  • Aceves, Seema S.2
  • Dellon, Evan S.3
  • Gupta, Sandeep K.4
  • Spergel, Jonathan M.5
  • Furuta, Glenn T.6
  • Rothenberg, Marc E.7
  • 1 Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH
  • 2 Division of Allergy Immunology, Center for Immunity, Infection and Inflammation, University of California San Diego and Rady Children's Hospital San Diego
  • 3 Division of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill, NC
  • 4 Division of Pediatric Gastroenterology, Hepatology and Nutrition, University of Illinois College of Medicine at Peoria and Children's Hospital of Illinois
  • 5 Division of Allergy and Immunology, The Children's Hospital of Philadelphia and Department of Pediatrics, Perelman School of Medicine at University of Pennsylvania
  • 6 Digestive Health Institute, Gastrointestinal Eosinophilic Diseases Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado and Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO
  • 7 Division of Allergy and Immunology, Department of Pediatrics Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH
Type
Published Article
Journal
Gastroenterology
Publication Date
Jul 27, 2017
Volume
154
Issue
2
Pages
333–345
Identifiers
DOI: 10.1053/j.gastro.2017.06.065
PMID: 28757265
PMCID: PMC5787048
Source
PubMed Central
Keywords
License
Unknown

Abstract

Eosinophilic esophagitis (EoE) is an emerging disease that is distinguished from gastroesophageal reflux disease (GERD) by the expression of a unique esophageal transcriptome and the interplay of early life environmental factors with distinct genetic susceptibility elements at 5q22 ( TSLP ) and 2p23 ( CAPN14 ). Rare genetic syndromes have uncovered the contribution of barrier disruption, mediated in part by defective desmosomes and dysregulated transforming factor beta (TGF-β) production and signaling, to EoE pathophysiology. Experimental modeling has defined a cooperative role of activated eosinophils, mast cells, and the cytokines IL-5 and IL-13, mediated by allergic sensitization to multiple foods. Understanding these processes is opening the way to better treatment based on disrupting allergic inflammatory and T helper type 2 cytokine–mediated responses including anti-cytokine therapeutics and dietary therapy.

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