Development and dysfunction of structural cells in eosinophilic esophagitis - 05/06/24
Abstract |
Eosinophilic esophagitis (EoE) is a disorder characterized by dysfunction and chronic local inflammation of the esophagus. The incidence and prevalence of EoE are increasing worldwide. The mechanisms responsible are poorly understood, and effective treatment options are limited. From the lumen outward, the esophagus comprises stratified squamous epithelium, lamina propria, and muscle. The tissue-specific nature of EoE strongly suggests that structural cells in the esophagus are involved in the EoE diathesis. Epithelial basal cell hyperplasia and dilated intercellular spaces are cardinal features of EoE. Some patients with EoE develop lamina propria fibrosis, strictures, or esophageal muscle dysmotility. Clinical symptoms of EoE are only weakly correlated with peak eosinophil count, implying that other cell types contribute to EoE pathogenesis. Epithelial, endothelial, muscle, and fibroblast cells can each initiate inflammation and repair, regulate tissue resident immune cells, recruit peripheral leukocytes, and tailor adaptive immune cell responses. A better understanding of how structural cells maintain tissue homeostasis, respond to cell-intrinsic and cell-extrinsic stressors, and exacerbate and/or resolve inflammatory responses in the esophagus is needed. This knowledge will facilitate the development of more efficacious treatment strategies for EoE that can restore homeostasis of both hematopoietic and structural elements in the esophagus.
Le texte complet de cet article est disponible en PDF.Key words : Esophagus, eosinophilic esophagitis, epithelium, basal cell hyperplasia, fibroblasts, endothelium
Abbreviations used : ANO, BCH, CSF, DIS, DSG, E-cadherin, ECM, EMT, EoE, FLIP, GERD, ILC2, LIGHT, LOX, LPF, MCP, NHE3, SMAD, PAI-1, PLN, POSTN, TLR, TRPV, TSLP, TSP-1, TSPAN12, YAP
Plan
Vol 153 - N° 6
P. 1485-1499 - juin 2024 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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