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Published in: Digestive Diseases and Sciences 5/2020

01-05-2020 | Chronic Inflammatory Bowel Disease | Original Article

A20 Restores Impaired Intestinal Permeability and Inhibits Th2 Response in Mice with Colitis

Authors: Donghui Chen, Li Ma, Tianyong Hu, Jiangqi Liu, Baohui Chen, Pingchang Yang, Zhiqiang Liu

Published in: Digestive Diseases and Sciences | Issue 5/2020

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Abstract

Background/Aims

The etiology of inflammatory bowel disease is multifactorial and still obscure. The protective role of ubiquitin E3 ligase A20 (A20) in colitis needs to be further elucidated. This study aimed to investigate whether A20 exogenous administration restored impaired intestinal permeability and inhibited T helper (Th)2 response in mice with colitis.

Methods

The effect of A20 overexpression in colonic mucosa on epithelial barrier function and T cell differentiation was evaluated in mice with dextran sulfate sodium (DSS)-induced chronic colitis.

Results

A20 rectal treatment alleviated DSS-induced chronic colitis and restored impaired intestinal permeability. Oral challenge with 2% DSS elicited a Th2-type response in mice with colitis, and A20 rectal treatment inhibited CD4+ interleukin (IL)-4+ T cell differentiation and proliferation. In addition, the RNA expressions of Th2-related costimulatory molecular T-cell immunoglobulin and mucin domain (TIM)-1 and IL-4 were suppressed, while thrombospondin (TSP)-1 and interferon (IFN)-γ expressions were upregulated, after A20 rectal administration.

Conclusion

A20 rectal treatment restores impaired intestinal permeability and inhibits activated Th2 cell response in mice with colitis.
Literature
Metadata
Title
A20 Restores Impaired Intestinal Permeability and Inhibits Th2 Response in Mice with Colitis
Authors
Donghui Chen
Li Ma
Tianyong Hu
Jiangqi Liu
Baohui Chen
Pingchang Yang
Zhiqiang Liu
Publication date
01-05-2020
Publisher
Springer US
Published in
Digestive Diseases and Sciences / Issue 5/2020
Print ISSN: 0163-2116
Electronic ISSN: 1573-2568
DOI
https://doi.org/10.1007/s10620-019-05860-8

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