Published online Nov 7, 2019. doi: 10.3748/wjg.v25.i41.6222
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
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.
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.
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.
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.
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.
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.
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.