Zheng CF, Shi JR, Huang Y, Wang SN. A20 inhibits lipopolysaccharide-induced inflammation in enterocytes. World J Gastrointest Pharmacol Ther 2016; 7(4): 540-549 [PMID: 27867687 DOI: 10.4292/wjgpt.v7.i4.540]
Corresponding Author of This Article
Ying Huang, MD, PhD, Department of Gastroenterology, Children’s Hospital of Fudan University, No. 399 Wan-Yuan Road, Minhang District, Shanghai 201102, China. yhuang815@163.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Pharmacol Ther. Nov 6, 2016; 7(4): 540-549 Published online Nov 6, 2016. doi: 10.4292/wjgpt.v7.i4.540
A20 inhibits lipopolysaccharide-induced inflammation in enterocytes
Cui-Fang Zheng, Jie-Ru Shi, Ying Huang, Sheng-Nan Wang
Cui-Fang Zheng, Jie-Ru Shi, Ying Huang, Sheng-Nan Wang, Department of Gastroenterology, Children’s Hospital of Fudan University, Shanghai 201102, China
Author contributions: Zheng CF and Huang Y designed the study; Zheng CF and Wang SN performed the research; Zheng CF and Shi JR analysed the data; Zheng CF, Shi JR and Huang Y wrote the paper.
Supported by The National Natural Science Foundation of China, No. 81300291.
Institutional review board statement: The publication of this manuscript has been reviewed and approved by the Children’s Hospital of Fudan University Review Board.
Conflict-of-interest statement: All authors declare no conflicts of interest.
Data sharing statement: The technical appendix, statistical code, and dataset are available from the corresponding author at yhuang815@163.com. The study participants provided their informed consent for data sharing. No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Ying Huang, MD, PhD, Department of Gastroenterology, Children’s Hospital of Fudan University, No. 399 Wan-Yuan Road, Minhang District, Shanghai 201102, China. yhuang815@163.com
Telephone: +86-21-64931727 Fax: +86-21-64931901
Received: May 1, 2016 Peer-review started: May 2, 2016 First decision: July 4, 2016 Revised: July 14, 2016 Accepted: August 15, 2016 Article in press: August 17, 2016 Published online: November 6, 2016 Processing time: 182 Days and 17.7 Hours
Core Tip
Core tip: The use of A20-deficient mice and RNA interference technologies has revealed that mice or enterocytes lacking A20 showed hyper-responsiveness to stimulation. However, studies on whether the overexpression of A20 can extenuate enterocyte inflammation are limited. Our present results demonstrated that the expression of A20 was increased in a dose- and time-dependent manner upon lipopolysaccharide (LPS) stimulation in intestinal epithelial cells. More importantly, the overexpression of A20 suppressed the activation of nuclear factor-κB and the induction of pro-inflammatory molecules, such as Tumor necrosis factor-α and IL-8. Taken together, these findings indicate that A20 plays a critical role in limiting LPS-induced inflammation in the gut luminal and may be a potential therapeutic tool for immune and inflammatory diseases.
