BPG is committed to discovery and dissemination of knowledge
Articles Published Processes
4/27/2018 3:25:40 AM | Browse: 1294 | Download: 2166
 |
Received |
|
2018-01-25 16:03 |
 |
Peer-Review Started |
|
2018-01-26 01:41 |
 |
First Decision by Editorial Office Director |
|
2018-02-23 20:56 |
 |
Return for Revision |
|
2018-02-27 01:44 |
 |
Revised |
|
2018-03-11 12:12 |
 |
Publication Fee Transferred |
|
|
 |
Second Decision by Editor |
|
2018-03-16 10:34 |
 |
Second Decision by Editor-in-Chief |
|
|
 |
Final Decision by Editorial Office Director |
|
2018-03-18 01:43 |
 |
Articles in Press |
|
2018-03-18 01:43 |
 |
Edit the Manuscript by Language Editor |
|
2018-03-28 20:31 |
 |
Typeset the Manuscript |
|
2018-04-25 11:11 |
 |
Publish the Manuscript Online |
|
2018-04-27 03:25 |
| ISSN |
1007-9327 (print) and 2219-2840 (online) |
| 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/ |
| Copyright |
© The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved. |
| Article Reprints |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
|
| Permissions |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
|
| Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
| Website |
http://www.wjgnet.com |
| Category |
Gastroenterology & Hepatology |
| Manuscript Type |
Basic Study |
| Article Title |
Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice
|
| Manuscript Source |
Unsolicited Manuscript |
| All Author List |
Hong-Xia Guo, Nan Ye, Ping Yan, Min-Yue Qiu, Ji Zhang, Zi-Gang Shen, Hai-Yang He, Zhi-Qiang Tian, Hong-Li Li and Jin-Tao Li |
| ORCID |
|
| Funding Agency and Grant Number |
| Funding Agency |
Grant Number |
| National Natural Science Foundation of China |
81271813 |
| National Natural Science Foundation of China |
81570497 |
|
| Corresponding Author |
Jin-Tao Li, PhD, Professor, Department of Preventive Medicine, Institute of Tropical Medicine, Gaotanyan Street 30, Shapingba District, Chongqing 400038, China. ljtqms@qq.com |
| Key Words |
NaCl; Inflammatory bowel disease; Macrophage; CD4+IFN-γ+IL-17+ T cell; p38/MAPK |
| Core Tip |
NaCl, as an indispensable environmental factor, evokes both innate and adaptive immune proinflammation cell activation in mice affected by dextran sulfate sodium (DSS)-induced colitis. Proinflammatory CD4+ cells in DSS- and NaCl-treated mice are mainly double-positive IL-17+IFN-γ+ T cells. Macrophage depletion significantly alleviates DSS-induced colitis. M1 macrophages play an important role in the proinflammatory effect of NaCl in the mouse gut. NaCl promotes M1 proinflammatory gene expression in lipopolysaccharide-activated peritoneal macrophage. The mechanism by which NaCl promotes DSS-induced colitis involves up-regulation of the p38/MAPK axis. |
| Publish Date |
2018-04-27 03:25 |
| Citation |
Guo HX, Ye N, Yan P, Qiu MY, Zhang J, Shen ZG, He HY, Tian ZQ, Li HL, Li JT. Sodium chloride exacerbates dextran sulfate sodium-induced colitis by tuning proinflammatory and antiinflammatory lamina propria mononuclear cells through p38/MAPK pathway in mice. World J Gastroenterol 2018; 24(16): 1779-1794 |
| URL |
http://www.wjgnet.com/1007-9327/full/v24/i16/1779.htm |
| DOI |
http://dx.doi.org/10.3748/wjg.v24.i16.1779 |
All content on this site: Copyright © 1993-2026 Baishideng Publishing Group Inc, its licensors, and contributors. All rights are reserved, including those for text and data mining, AI training, and similar technologies. For all open access content, the relevant licensing terms apply.