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©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 7, 2017; 23(21): 3850-3863
Published online Jun 7, 2017. doi: 10.3748/wjg.v23.i21.3850
Published online Jun 7, 2017. doi: 10.3748/wjg.v23.i21.3850
Sodium selenite ameliorates dextran sulfate sodium-induced chronic colitis in mice by decreasing Th1, Th17, and γδT and increasing CD4(+)CD25(+) regulatory T-cell responses
Li-Xuan Sang, Jun-Feng Zhu, Fang-Li Yang, Yan Li, Xue-Feng Jiang, Da-Nan Wang, Chang-Long Lu, Xun Sun, Department of Immunology, China Medical University, Shenyang 110122, Liaoning Province, China
Li-Xuan Sang, Department of Geriatrics, First Affiliated Hospital, China Medical University, Shenyang 110001, Liaoning Province, China
Bing Chang, Department of Gastroenterology, First Affiliated Hospital, China Medical University, Shenyang 110001, Liaoning Province, China
Author contributions: Wang DN and Lu CL are the co-corresponding authors; Sang LX, Chang B and Sun X performed the experiments, analyzed and interpreted the data, and wrote the manuscript; Jiang XF, Yang FL, and Li Y performed animal experiments and molecular biology experiments; Wang DN and Lu CL conceived the study; all authors approved the final manuscript.
Supported by National Natural Science Foundation of China , No. 31370921 ; and Natural Science Foundation of Liaoning Province , No. 2015020515 .
Institutional review board statement: All specimens from the mice were taken after ethical permission was obtained for participation in the study.
Institutional animal care and use committee statement: The experimental protocols were approved by Institutional Animal Care and Use Committee of China Medical University.
Conflict-of-interest statement: The authors disclose no potential competing interests.
Data sharing statement: 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: Dr. Chang-Long Lu, Professor, Department of Immunology, China Medical University, No. 77, Puhe Road, Shenyang North New Area, Shenyang 110122, Liaoning Province, China. cllu@mail.cmu.edu.cn
Telephone: +86-24-83283764 Fax: +86-24-83283765
Received: October 19, 2016
Peer-review started: October 21, 2016
First decision: November 9, 2016
Revised: December 29, 2016
Accepted: March 15, 2017
Article in press: March 15, 2017
Published online: June 7, 2017
Processing time: 230 Days and 8.2 Hours
Peer-review started: October 21, 2016
First decision: November 9, 2016
Revised: December 29, 2016
Accepted: March 15, 2017
Article in press: March 15, 2017
Published online: June 7, 2017
Processing time: 230 Days and 8.2 Hours
Core Tip
Core tip: Se significantly ameliorated the symptoms of colitis and histological injury, increasing the proportions of neutrophils and CD4+ CD25+ T cells and decreasing the proportions of γδT cells, CD4+, CD4+CD44+, and CD4+ CD69+ T cells in LPL. Moreover, Se reduced the expression of IL-6, IFN-γ, IL-17A, IL-21, T-bet, and RORγt, but enhanced the expression of IL-10 and Foxp3. The study suggests that Se protects against DSS-induced chronic colitis perhaps by increasing the number of CD4(+)CD25(+) Tregs that suppress the secretion of proinflammatory cytokines and populations of Th1, Th17, and γδT cells.