Abstract
The clinical and pathologic features of eosinophilic esophagitis (EE) include extensive tissue remodeling. Increasing evidence supports a key role for the eosinophil in multiple aspects of the esophageal remodeling and fibrosis seen in this allergic disease. This article reviews the clinical implications of esophageal remodeling and fibrosis in EE and discusses the possible pathogenic mechanisms inducing and regulating these responses. The focus is specifically on eosinophil and cytokine interactions with the esophageal epithelium, vascular endothelium, resident fibroblasts, and smooth muscle. Current and potential therapeutic interventions are discussed that may impact the development or resolution of chronic esophageal remodeling and fibrosis in EE.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Cell Communication
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Cell Movement
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Cell Survival
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Chemotactic Factors, Eosinophil / immunology
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Endothelial Cells / immunology
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Endothelial Cells / metabolism
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Endothelial Cells / pathology
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Eosinophilia / complications
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Eosinophilia / immunology*
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Eosinophilia / metabolism
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Eosinophilia / pathology
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Eosinophils / immunology
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Eosinophils / metabolism*
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Eosinophils / pathology
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Esophagitis / complications
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Esophagitis / immunology*
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Esophagitis / metabolism
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Esophagitis / pathology
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Fibroblasts / immunology
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Fibroblasts / metabolism
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Fibroblasts / pathology
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Fibrosis / immunology
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Humans
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Hypersensitivity / complications
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Hypersensitivity / immunology*
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Hypersensitivity / metabolism
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Hypersensitivity / pathology
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Inflammation
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Intestinal Mucosa / immunology
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Intestinal Mucosa / metabolism*
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Intestinal Mucosa / pathology
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Nerve Growth Factors / immunology
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Transforming Growth Factor beta / immunology
Substances
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Chemotactic Factors, Eosinophil
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Nerve Growth Factors
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Transforming Growth Factor beta