Type 2 Inflammation in Eosinophilic Esophagitis: From Pathophysiology to Therapeutic Targets.
eosinophilic esophagitis
pathophysiology
precision medicine
therapeutic targets
type 2 inflammation
Journal
Frontiers in physiology
ISSN: 1664-042X
Titre abrégé: Front Physiol
Pays: Switzerland
ID NLM: 101549006
Informations de publication
Date de publication:
2021
2021
Historique:
received:
15
11
2021
accepted:
09
12
2021
entrez:
31
1
2022
pubmed:
1
2
2022
medline:
1
2
2022
Statut:
epublish
Résumé
Eosinophilic esophagitis (EoE) is a chronic immune-mediated disease of the esophagus characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation, whose incidence is rising. It significantly affects patients' quality of life and, if left untreated, results in fibrotic complications. Although broad consensus has been achieved on first-line therapy, a subset of patients remains non-responder to standard therapy. The pathogenesis of EoE is multifactorial and results from the complex, still mostly undefined, interaction between genetics and intrinsic factors, environment, and antigenic stimuli. A deep understanding of the pathophysiology of this disease is pivotal for the development of new therapies. This review provides a comprehensive description of the pathophysiology of EoE, starting from major pathogenic mechanisms (genetics, type 2 inflammation, epithelial barrier dysfunction, gastroesophageal reflux, allergens, infections and microbiota) and subsequently focusing on the single protagonists of type 2 inflammation (involved cells, cytokines, soluble effectors, surface proteins and transcription factors) that could represent present and future therapeutic targets, while summarizing previous therapeutic approaches in literature.
Identifiants
pubmed: 35095572
doi: 10.3389/fphys.2021.815842
pmc: PMC8790151
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
815842Informations de copyright
Copyright © 2022 Racca, Pellegatta, Cataldo, Vespa, Carlani, Pelaia, Paoletti, Messina, Nappi, Canonica, Repici and Heffler.
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. The handling editor declared a past collaboration with several of the authors GWC and EH.
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