MicroRNA Modulation of Host Immune Response and Inflammation Triggered by Helicobacter pylori
Maria Oana Săsăran1, Lorena Elena Meliț2, Ecaterina Daniela Dobru3
1Department of Pediatrics III, "George Emil Palade" University of Medicine, Pharmacy, Sciences and Technology of Târgu Mureș, Gheorghe Marinescu Street no 38, 540136 Târgu Mureș, Romania.
Abstract:
Helicobacter pylori (H. pylori) remains the most-researched etiological factor for gastric inflammation and malignancies. Its evolution towards gastric complications is dependent upon host immune response. Toll-like receptors (TLRs) recognize surface and molecular patterns of the bacterium, especially the lipopolysaccharide (LPS), and act upon pathways, which will finally lead to activation of the nuclear factor-kappa B (NF-kB), a transcription factor that stimulates release of inflammatory cytokines. MicroRNAs (MiRNAs) finely modulate TLR signaling, but their expression is also modulated by activation of NF-kB-dependent pathways. This review aims to focus upon several of the most researched miRNAs on this subject, with known implications in host immune responses caused by H. pylori, including let-7 family, miRNA-155, miRNA-146, miRNA-125, miRNA-21, and miRNA-221. TLR-LPS interactions and their afferent pathways are regulated by these miRNAs, which can be considered as a bridge, which connects gastric inflammation to pre-neoplastic and malignant lesions. Therefore, they could serve as potential non-invasive biomarkers, capable of discriminating H. pylori infection, as well as its associated complications. Given that data on this matter is limited in children, as well as for as significant number of miRNAs, future research has yet to clarify the exact involvement of these entities in the progression of H. pylori-associated gastric conditions.
Insights
Helicobacter pylori (H. pylori) infection triggers immune responses involving Toll-like receptors (TLRs) and microRNAs (miRNAs). These miRNAs may serve as biomarkers for H. pylori-related gastric inflammation and cancer.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Helicobacter pylori (H. pylori) is a primary cause of gastric inflammation and cancer.
- Host immune responses, particularly involving Toll-like receptors (TLRs), are crucial in H. pylori pathogenesis.
- MicroRNAs (miRNAs) play a regulatory role in immune signaling pathways affected by H. pylori.
Purpose of the Study:
- To review key miRNAs involved in H. pylori-induced immune responses.
- To explore the role of miRNAs in connecting H. pylori infection to gastric inflammation and malignancy.
- To assess the potential of miRNAs as non-invasive biomarkers for H. pylori infection and its complications.
Main Methods:
- Literature review focusing on H. pylori, TLRs, NF-kB, and specific miRNAs (let-7 family, miR-155, miR-146, miR-125, miR-21, miR-221).
- Analysis of the regulatory interactions between TLR-LPS pathways and miRNA expression.
- Synthesis of current knowledge on miRNA involvement in H. pylori-associated gastric conditions.
Main Results:
- Specific miRNAs (let-7 family, miR-155, miR-146, miR-125, miR-21, miR-221) modulate TLR signaling in response to H. pylori.
- These miRNAs act as a link between H. pylori-induced inflammation and the development of pre-neoplastic and malignant gastric lesions.
- Evidence suggests miRNAs could be potential non-invasive biomarkers for H. pylori infection and associated pathologies.
Conclusions:
- MiRNAs are critical regulators of the host immune response to H. pylori, influencing gastric inflammation and cancer progression.
- Targeting these miRNAs may offer therapeutic strategies for H. pylori-related diseases.
- Further research, especially in pediatric populations, is needed to fully elucidate the role of miRNAs in H. pylori-associated gastric conditions.
More Related Videos
Related Concept Videos
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
MicroRNAs
MicroRNAs
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
Gene Regulation in Microbial Communities: Quorum Sensing


