Eosinophils in Eosinophilic Esophagitis: The Road to Fibrostenosis is Paved With Good Intentions.
Administration, Oral
Allergens
/ administration & dosage
Animals
Antigens
/ immunology
Desensitization, Immunologic
/ adverse effects
Disease Progression
Eosinophilic Esophagitis
/ immunology
Eosinophils
/ immunology
Esophageal Stenosis
/ immunology
Esophagus
/ immunology
Fibrosis
Food Hypersensitivity
/ immunology
Humans
Risk Factors
Signal Transduction
eosinophil
eosinophilic esophagitis
epithelial barrier
esophagus
fibrosis
food allergy
oral immunotherapy
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
06
09
2020
accepted:
03
11
2020
entrez:
18
12
2020
pubmed:
19
12
2020
medline:
22
6
2021
Statut:
epublish
Résumé
Eosinophilic esophagitis (EoE) is an antigen-driven disease associated with epithelial barrier dysfunction and chronic type 2 inflammation. Eosinophils are the defining feature of EoE histopathology but relatively little is known about their role in disease onset and progression. Classically defined as destructive, end-stage effector cells, eosinophils (a resident leukocyte in most of the GI tract) are increasingly understood to play roles in local immunity, tissue homeostasis, remodeling, and repair. Indeed, asymptomatic esophageal eosinophilia is observed in IgE-mediated food allergy. Interestingly, EoE is a potential complication of oral immunotherapy (OIT) for food allergy. However, we recently found that patients with peanut allergy may have asymptomatic esophageal eosinophilia at baseline and that peanut OIT induces transient esophageal eosinophilia in most subjects. This is seemingly at odds with multiple studies which have shown that EoE disease severity correlates with tissue eosinophilia. Herein, we review the potential role of eosinophils in EoE at different stages of disease pathogenesis. Based on current literature we suggest the following: (1) eosinophils are recruited to the esophagus as a homeostatic response to epithelial barrier disruption; (2) eosinophils mediate barrier-protective activities including local antibody production, mucus production and epithelial turnover; and (3) when type 2 inflammation persists, eosinophils promote fibrosis.
Identifiants
pubmed: 33335531
doi: 10.3389/fimmu.2020.603295
pmc: PMC7736408
doi:
Substances chimiques
Allergens
0
Antigens
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
603295Subventions
Organisme : NIAID NIH HHS
ID : U54 AI117804
Pays : United States
Organisme : NCATS NIH HHS
ID : U2C TR002818
Pays : United States
Informations de copyright
Copyright © 2020 Doyle, Masuda, Kita and Wright.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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