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Molecular, genetic, and cellular bases for treating eosinophilic esophagitis.

Abstract：

:Eosinophilic esophagitis (EoE) was historically distinguished from gastroesophageal reflux disease on the basis of histology and lack of responsiveness to acid suppressive therapy, but it is now appreciated that esophageal eosinophilia can respond to proton pump inhibitors. Genetic and environmental factors contribute to risk for EoE, particularly early-life events. Disease pathogenesis involves activation of epithelial inflammatory pathways (production of eotaxin-3 [encoded by CCL26]), impaired barrier function (mediated by loss of desmoglein-1), increased production and/or activity of transforming growth factor-β, and induction of allergic inflammation by eosinophils and mast cells. Susceptibility has been associated with variants at 5q22 (TSLP) and 2p23 (CAPN14), indicating roles for allergic sensitization and esophageal specific protease pathways. We propose that EoE is a unique disease characterized by food hypersensitivity; strong hereditability influenced by early-life exposures and esophageal-specific genetic risk variants; and allergic inflammation and that the disease is remitted by disrupting inflammatory and T-helper type 2 cytokine-mediated responses and through dietary elimination therapy.

journal_name

Gastroenterology

journal_title

Gastroenterology

authors

Rothenberg ME

doi

10.1053/j.gastro.2015.02.002

subject

Has Abstract

pub_date

2015-05-01 00:00:00

pages

1143-57

issue

6

eissn

0016-5085

issn

1528-0012

pii

S0016-5085(15)00165-1

journal_volume

148

pub_type

杂志文章,评审

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