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

• Published in: International journal of molecular sciences Vol. 22; no. 3; p. 1406
• Main Authors: Săsăran, Maria Oana, Meliț, Lorena Elena, Dobru, Ecaterina Daniela
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 30.01.2021; MDPI
• Subjects: Ammonia; Biofilms; Cell cycle; Cell growth; Cytokines; Enzymes; Gene expression; Immune response; Infections; Inflammation; MicroRNAs; Neutrophils; Pathogens; Protein synthesis; Proteins; Review; Virulence; host immune response; miRNA; H. pylori; TLR; gastric inflammation
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms22031406

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.