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IL-33 is induced in undifferentiated, non-dividing esophageal epithelial cells in eosinophilic esophagitis.

IL-33 is induced in undifferentiated, non-dividing esophageal epithelial cells in eosinophilic esophagitis.
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Travers J, Rochman M, Caldwell JM, Besse JA, Miracle CE, Rothenberg ME,


Travers J, Rochman M, Caldwell JM, Besse JA, Miracle CE, Rothenberg ME, (click to view)

Travers J, Rochman M, Caldwell JM, Besse JA, Miracle CE, Rothenberg ME,

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Scientific reports 2017 12 147(1) 17563 doi 10.1038/s41598-017-17541-5
Abstract

The molecular and cellular etiology of eosinophilic esophagitis (EoE), an emerging tissue-specific allergic disease, involves dysregulated gene expression in esophageal epithelial cells. Herein, we assessed the esophageal expression of IL-33, an epithelium-derived alarmin cytokine, in patients with EoE. IL-33 protein was markedly overexpressed within the nuclei of a subpopulation of basal layer esophageal epithelial cells in patients with active EoE compared to control individuals. IL-33 exhibited dynamic expression as levels normalized upon EoE remission. IL-33-positive basal epithelial cells expressed E-cadherin and the undifferentiated epithelial cell markers keratin 5 and 14 but not the differentiation marker keratin 4. Moreover, the IL-33-positive epithelial cells expressed the epithelial progenitor markers p75 and p63 and lacked the proliferation markers Ki67 and phospho-histone H3. Additionally, the IL-33-positive cells had low expression of PCNA. IL-33 expression was detected in ex vivo-cultured primary esophageal epithelial cells in a subpopulation of cells lacking expression of proliferation markers. Collectively, we report that IL-33 expression is induced in an undifferentiated, non-dividing esophageal epithelial cell population in patients with active EoE.

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