MicroRNA Modulation of Host Immune Response and Inflammation Triggered by Helicobacter pylori

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.

Automated summary

Helicobacter pylori is the most researched etiological factor for gastric inflammation and malignancies, with Toll-like receptors playing a key role in recognizing the bacterium. MicroRNAs modulate TLR signaling and are regulated by NF-κB-dependent pathways. Certain MiRNAs can potentially serve as non-invasive biomarkers for discriminating H. pylori infection and associated complications, connecting gastric inflammation to pre-neoplastic and malignant lesions. Further research is needed to clarify the exact involvement of these entities in the progression of H. pylori-associated gastric conditions, especially in children.