Eosinophilic esophagitis is a chronic disease whose incidence and prevalence are increasing, based on a genetic-driven interaction between environment and immune system. Several gene loci involved in the development of the disease have been identified. A two-step mechanism has been hypothesized: a TSLP-induced allergic sensitization followed by upregulation of CAPNA14-related esophageal-specific pathways. Environment seems to have a larger effect than genetic variants. Factors that could play a role are allergens, drugs, colonizing bacteria and possibly Helicobacter Pylori infection. Acting on these modifiable risk factors may be a tool to prevent the disease. EoE is characterized by a typical eosinophilic infiltrate limited to the esophageal epithelium, supported by a Th2-mediated immune response, found in other atopic conditions. The key of the pathogenesis is the disfunction of the epithelial barrier which allow the interaction between allergens and inflammatory cells. Eosinophilic-predominant inflammation leads to the typical wall remodeling, histologically characterized by epithelial and smooth muscle hyperplasia, lamina propria fibrosis and neo-angiogenesis. These alterations find their clinical expression in the pattern of symptoms: dysphagia, food impaction, chest pain, heartburn.

Eosinophilic esophagitis: novel concepts regarding pathogenesis and clinical manifestations

Visaggi, Pierfrancesco
Secondo
Writing – Original Draft Preparation
;
Sostilio, Andrea
Writing – Original Draft Preparation
;
Tarducci, Luca
Writing – Original Draft Preparation
;
Pugno, Camilla
Membro del Collaboration Group
;
Ricchiuti, Angelo
Membro del Collaboration Group
;
Bellini, Massimo
Membro del Collaboration Group
;
Marchi, Santino
Membro del Collaboration Group
;
De Bortoli, Nicola
Ultimo
Writing – Review & Editing
2021-01-01

Abstract

Eosinophilic esophagitis is a chronic disease whose incidence and prevalence are increasing, based on a genetic-driven interaction between environment and immune system. Several gene loci involved in the development of the disease have been identified. A two-step mechanism has been hypothesized: a TSLP-induced allergic sensitization followed by upregulation of CAPNA14-related esophageal-specific pathways. Environment seems to have a larger effect than genetic variants. Factors that could play a role are allergens, drugs, colonizing bacteria and possibly Helicobacter Pylori infection. Acting on these modifiable risk factors may be a tool to prevent the disease. EoE is characterized by a typical eosinophilic infiltrate limited to the esophageal epithelium, supported by a Th2-mediated immune response, found in other atopic conditions. The key of the pathogenesis is the disfunction of the epithelial barrier which allow the interaction between allergens and inflammatory cells. Eosinophilic-predominant inflammation leads to the typical wall remodeling, histologically characterized by epithelial and smooth muscle hyperplasia, lamina propria fibrosis and neo-angiogenesis. These alterations find their clinical expression in the pattern of symptoms: dysphagia, food impaction, chest pain, heartburn.
2021
Sciumé, Giusi D; Visaggi, Pierfrancesco; Sostilio, Andrea; Tarducci, Luca; Pugno, Camilla; Frazzoni, Marzio; Ricchiuti, Angelo; Bellini, Massimo; Gian...espandi
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/1111393
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