Basic Study
Copyright ©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Nov 7, 2019; 25(41): 6222-6237
Published online Nov 7, 2019. doi: 10.3748/wjg.v25.i41.6222
MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori
Jing Feng, Jian Guo, Jun-Ping Wang, Bao-Feng Chai
Jing Feng, Bao-Feng Chai, Institute of Loess Plateau, Shanxi University, Taiyuan 030006, Shanxi Province, China
Jing Feng, Jun-Ping Wang, Department of Gastroenterology, Shanxi Provincial People's Hospital, The Affiliated People's Hospital of Shanxi Medical University, Taiyuan 030012, Shanxi Province, China
Jian Guo, Department of General Surgery, Shanxi Provincial People's Hospital, The Affiliated People's Hospital of Shanxi Medical University, Taiyuan 030012, Shanxi Province, China
Author contributions: Chai BF and Wang JP designed the research; Feng J and Guo J performed the research; Feng J and Chai BF analyzed the data; Feng J and Wang JP wrote the paper.
Institutional review board statement: The study was reviewed and approved by the Ethics Committee of Shanxi University and Ethics Committee of Shanxi Provincial People's Hospital, Shanxi Province, China.
Conflict-of-interest statement: There was no competing interest.
Data sharing statement: All the data in the current research are available from the corresponding author on reasonable request.
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: Bao-Feng Chai, MD, PhD, Professor, Institute of Loess Plateau, Shanxi University, No. 92, Wucheng Road, Taiyuan 030006, Shanxi Province, China. 13644359409@163.com
Telephone: +86-13603583312
Received: January 26, 2019
Peer-review started: August 27, 2019
First decision: September 19, 2019
Revised: October 11, 2019
Accepted: October 22, 2019
Article in press: October 22, 2019
Published online: November 7, 2019
ARTICLE HIGHLIGHTS
Research background

Helicobacter pylori (H. pylori) infection is a global issue that could cause a variety of diseases involving multiple organs. It is worth noting that the incidence of H. pylori-related enteritis in children increases, but the underlying mechanism is largely unknown. It has been reported that miR-32-5p is overexpressed in diseases associated with bacterial infection. However, the potential role of miR-32-5p in H. pylori-induced pediatric enteritis is not clear.

Research motivation

To investigate the exact role of miR-32-5p in the pathogenesis of pediatric enteritis with H. pylori infection, and to find a novel target for H. pylori-related enteritis in children.

Research objectives

To explore the aberrant expression and significance of miR-32-5p in children with H. pylori-related enteritis, especially in the damage of intestinal epithelial cells with H. pylori infection.

Research methods

qRT-PCR was performed to detect the expression of miR-32-5p in clinical samples and H. pylori-infected intestinal epithelial cells. Cell Counting Kit-8 assay and flow cytometry were conducted to evaluate the role of miR-32-5p in H. pylori-infected intestinal epithelial cells. TargetScanHuman database and luciferase assay were utilized to verify the potential target of miR-32-5p. Western blot was employed to clarify the underlying mechanism of miR-32-5p in influencing H. pylori-infected intestinal epithelial cells.

Research results

The present study discovered the aberrant expression of miR-32-5p in pediatric enteritis with H. pylori infection and H. pylori-treated intestinal epithelial cells. The in vitro experiments showed the significance of miR-32-5p in regulating cell viability and apoptosis of H. pylori-treated intestinal epithelial cells. We identified that SMAD family member 6 (SMAD6) was the direct target of miR-32-5p, and SMAD6 partially counteracted the harmful role of miR-32-5p by inhibiting the activation of TAK1-p38 cascade. However, in vivo assays are needed to further verify our in vitro findings and significance of miR-32-5p in H. pylori-induced pediatric enteritis.

Research conclusions

Our research first identified the upregulation of miR-32-5p in H. pylori-related pediatric enteritis. Further exploration revealed that miR-32-5p inhibited SMAD6 to activate the TAK1-p38 signaling pathway, aggravating H. pylori-induced damage of intestinal epithelial cells. MiR-32-5p might be a potential target to overcome H. pylori-induced damage of intestinal epithelial cells in children.

Research perspectives

Based on the clinical findings and in vitro experiments, miR-32-5p could be a novel therapeutic target for H. pylori-induced damage of intestinal epithelial cells in children. Further in vivo assays are of necessity to clarify the deleterious effects of miR-32-5p on H. pylori-infected intestinal epithelial cells, which is very meaningful and would contribute to clinical application.