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Updated: Apr 16, 2026
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
miR-155 and miR-146b negatively regulates IL6 in Helicobacter pylori (cagA+) infected gastroduodenal ulcer
1Emergency Department, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shanxi, China. chengsanfang@sina.com.
Objective:
Helicobacter pylori (H. pylori) infection is the main cause of gastroduodenal ulcer. The molecular mechanisms that underlying this progress are still not very clear. MicroRNAs (miRNAs) are small noncoding RNAs that function as negative regulator of numerous target genes at posttranscriptional level. miRNAs plays important roles in the development of many infection related diseases. The roles of miRNAs in the development of H. pylori-infected gastroduodenal ulcer haven't been well studied yet.
Materials And Methods:
The miRNA and mRNA profiles in normal gastroduodenal biopsy, H. pylori-infected gastroduodenal biopsy and H. pylori-infected gastroduodenal ulcer biopsy samples were compared and analyzed to identify potential related miRNAs and their target genes. The differential expression of the identified miRNAs and their target gene were validated in an independent set of H. pylori positive gastroduodenal ulcer biopsy samples by immunohistochemistry staining and RT-PCR. Then microRNA mimics were transfected to gastric epithelial cells infected with H. pylori 26695 (cagA+). RT-PCR and Western blotting were performed to confirm the target gene of the identified microRNAs.
Results:
The integrative analysis and immunohistochemistry staining validation indicated that miR-155 and miR-146b, as well as their predicted target gene IL6, are up-regulated in H. pylori positive gastroduodenal ulcer. Further experiments in gastric epithelial cells revealed that H. pylori 26695 (cagA+) infection induces IL6 overexpression. But the overexpression of IL6 is weaken due to negative regulation by miR-155 and miR-146b.
Conclusions:
This study indicated that the up-regulation of miR-155 and miR-146b decreases H. pylori (cagA+)-introduced IL6 overexpression, which might weaken the cleanup of H. pylori (cagA+) and contributes to ulcer.
Insights
MicroRNAs miR-155 and miR-146b are upregulated in Helicobacter pylori (H. pylori) infections, reducing IL6 overexpression and potentially contributing to gastroduodenal ulcers. This finding offers new insights into H. pylori pathogenesis.
Area of Science:
- Molecular biology
- Gastroenterology
- Microbiology
Background:
- Helicobacter pylori (H. pylori) infection is a primary cause of gastroduodenal ulcers, but underlying molecular mechanisms remain unclear.
- MicroRNAs (miRNAs) are key post-transcriptional regulators involved in various diseases, yet their role in H. pylori-induced ulcers is understudied.
Purpose of the Study:
- To investigate the roles of miRNAs in the pathogenesis of H. pylori-infected gastroduodenal ulcers.
- To identify specific miRNAs and their target genes involved in the development of H. pylori-related gastroduodenal pathology.
Main Methods:
- Comparative analysis of miRNA and mRNA profiles in normal, H. pylori-infected, and ulcer biopsy samples.
- Validation of differential miRNA and target gene expression using immunohistochemistry and RT-PCR.
- In vitro experiments involving miRNA mimic transfection in H. pylori-infected gastric epithelial cells, followed by RT-PCR and Western blotting.
Main Results:
- miR-155 and miR-146b were found to be upregulated in H. pylori-positive gastroduodenal ulcers.
- Interleukin-6 (IL6) was identified as a target gene, showing upregulation in infected tissues.
- H. pylori infection induced IL6 overexpression, which was subsequently attenuated by the negative regulation of miR-155 and miR-146b.
Conclusions:
- Upregulation of miR-155 and miR-146b mitigates H. pylori-induced IL6 overexpression.
- This miRNA-mediated regulation may impair bacterial clearance, contributing to the development of gastroduodenal ulcers.
- The findings highlight a novel miRNA-based mechanism in H. pylori pathogenesis.
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