Basic Study
Copyright ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 7, 2019; 25(45): 6634-6652
Published online Dec 7, 2019. doi: 10.3748/wjg.v25.i45.6634
Toxoplasma ROP16I/III ameliorated inflammatory bowel diseases via inducing M2 phenotype of macrophages
Yong-Wei Xu, Rui-Xin Xing, Wen-Hui Zhang, Lu Li, Yi Wu, Jing Hu, Cong Wang, Qing-Li Luo, Ji-Long Shen, Xi Chen
Yong-Wei Xu, Rui-Xin Xing, Wen-Hui Zhang, Lu Li, Yi Wu, Jing Hu, Xi Chen, Department of Gastroenterology, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui Province, China
Cong Wang, Qing-Li Luo, Ji-Long Shen, Department of Pathogen Biology, Provincial Laboratory of Pathogen Biology and Zoonoses Anhui, Anhui Medical University, Hefei 230032, Anhui Province, China
Author contributions: Chen X, Sheng JL and Xu YW conceived and designed the trial; Xu YW, Li L, Xing RX and Wu Y performed the experiments; Xu YW, Zhang WH, Hu J, Wang C and Luo QL analysed the data; Xu YW wrote the manuscript; Chen X, Sheng JL and Xu YW critically revised the manuscript; All authors have read and approved the final manuscript.
Supported by the National Natural Science Foundation of China, No. 81471983; the Key Research and Development Plan Project of Anhui Province, Department of Science and Technology 2019, No. 201904a07020043; the Key Project of Natural Science Research in the Universities of Anhui Provence, No. KJ2017A202; and the Research Fund Project of Anhui Institute of Transforming Medicine, No. 2017zhyx04.
Institutional review board statement: This study does not involve human and animal subjects.
Institutional animal care and use committee statement: No animal models were used in this study.
Conflict-of-interest statement: None of the authors has any conflicts of interest to declare.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The ARRIVE guidelines have been adopted.
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/
Corresponding author: Xi Chen, MD, PhD, Chief Doctor, Dean, Director, Professor, Senior Researcher, Department of Gastroenterology, the First Affiliated Hospital of Anhui Medical University, No. 218 Ji Xi Road, Hefei 230022, Anhui Province, China. ayfychenxi@163.com
Telephone: +86-551-65908802 Fax: +86-551-65908802
Received: August 9, 2019
Peer-review started: August 9, 2019
First decision: September 19, 2019
Revised: October 3, 2019
Accepted: November 13, 2019
Article in press: November 13, 2019
Published online: December 7, 2019
Processing time: 118 Days and 22.1 Hours
Core Tip

Core tip:Toxoplasma ROP16I/III (ToxoROP16I/III) induced RAW264.7 polarization to M2 macrophage, down-regulated the M1-associated inflammation response and protective Caco-2 intestinal epithelial cells. ToxoROP16I/III can phosphorylate and activate the transcription factors signal transducer and activator of signal transducer and activator of transcription (Stat) 3 and Stat6, promote the polarization of M2 cells, and enhance the synthesis of arginase-1, interleukin (IL)-10, transforming growth factor-β1, and IL-13. The IL-1β, TNF-α, IL-6, nitric oxide (NO), and inducible nitric oxide synthase(iNOS)produced by M1 cells were notably downregulated when the ToxoROP16I/III-induced M2 macrophages were added to the mixture of culture.Co-culture with Caco-2 cells through transwell alleviated Caco-2 cell apoptosis and caspase-3, -8, and -9 associated proteins. This study aims to confirm that ToxoROP16I/III may provide a novel strategy for IBD immuno-therapy with parasite-derived effector molecules.