Basic Study
Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 14, 2017; 23(6): 999-1009
Published online Feb 14, 2017. doi: 10.3748/wjg.v23.i6.999
Effect of toll-like receptor 3 agonist poly I:C on intestinal mucosa and epithelial barrier function in mouse models of acute colitis
Hong-Wei Zhao, Yue-Hong Yue, Hua Han, Xiu-Li Chen, Yong-Gang Lu, Ji-Min Zheng, Hong-Tao Hou, Xiao-Meng Lang, Li-Li He, Qi-Lu Hu, Zi-Qian Dun
Hong-Wei Zhao, Ji-Min Zheng, Hong-Tao Hou, Department of Gastroenterology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China
Yue-Hong Yue, Department of Neurology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China
Hua Han, Department of Obstetrics and Gynecology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China
Xiu-Li Chen, Research Center, The Fifth Hospital of Shijiazhuang, Shijiazhuang 050021, Hebei Province, China
Yong-Gang Lu, Department of Clinical Laboratory, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China
Xiao-Meng Lang, Department of Spleen and Stomach, Hebei Province Hospital of Traditional Chinese Medicine, Shijiazhuang 500011, Hebei Province, China
Li-Li He, Department of Gerontology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China
Qi-Lu Hu, Department of Oncology, Hebei General Hospital, Shijiazhuang 050051, Hebei Province, China
Zi-Qian Dun, Department of General Internal Medicine, The Fifth Hospital of Shijiazhuang, Shijiazhuang 050021, Hebei Province, China
Author contributions: Zhao HW, Yue YH, Han H, Chen XL and Lu YG participated in study design, experiment performance, data interpretation and manuscript revision and coordination; Zheng JM, Hou HT and Lang XM contributed to experiment performance, data collection and manuscript drafting; He LL, Hu QL and Dun ZQ worked on experiment performance and manuscript revision; all authors contributed significantly to this work.
Supported by the Scientific Research Foundation of Health Department of Hebei Province, No. 20160483.
Institutional review board statement: This work was approved by the Institutional Review Board of Hebei General Hospital.
Institutional animal care and use committee statement: All animal experiments were reviewed and approved by the Institutional Animal Care and Use Committee (IACUC, Approval ID: I07-038-3).
Conflict-of-interest statement: The authors declare no conflict of interest.
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: Hong-wei Zhao, MD, Department of Gastroenterology, Hebei General Hospital, No.348 Hepingxi Road, Shijiazhuang 050051, Hebei Province, China. hongweizhao788@163.com
Telephone: +86-13303039680 Fax: +86-311-85988449
Received: August 17, 2016
Peer-review started: August 19, 2016
First decision: September 6, 2016
Revised: September 26, 2016
Accepted: October 30, 2016
Article in press: October 31, 2016
Published online: February 14, 2017
Processing time: 178 Days and 22.4 Hours
Core Tip

Core tip: Poly I:C, a toll-like receptor 3 agonist, has been previously reported to protect against acute colitis. The potential effects of poly I:C on mucosal injury and epithelial barrier disruption were investigated in mouse models of dextran sulfate sodium (DSS)-induced acute colitis. Poly I:C administration dramatically protected against DSS-induced colitis, with ameliorated ultrastructural changes of colon epithelium, intestinal permeability and tight junction protein expressions. Poly I:C may protect against DSS-induced colitis through maintaining integrity of the epithelial barrier and regulating innate immune responses.