MicroRNA-146a inhibits the inflammatory responses induced by interleukin-17A during the infection of Helicobacter pylori

Helicobacter pylori (H. pylori) infection is the major cause of chronic active gastritis and peptic ulcer disease. Upregulation of IL-17A is associated with H. pylori infection in the gastric mucosa; however, the factors involved in the regulation of interleukin (IL)-17A-induced inflammatory responses in H. pylori-associated gastritis remain unknown. MicroRNAs (miRNAs) serve as key post-transcriptional regulators of gene expression and are associated with the H. pylori infection. The present study aimed to analyze the effects of IL-17A on the expression of miR-146a upon infection with H. pylori, as well as to identify the possible impact of miR-146a dysregulation on the inflammatory response in vivo and in vitro. Reverse transcription-quantitative polymerase chain reaction analysis was used to determine the expression levels of miR-146a in gastric epithelial cells upon IL-17A stimulation. The effects of miR-146a mimics on IL-17A-induced inflammatory responses in SGC-7901 cells were evaluated. The effects of miR-146a mimics on the expression levels of IL-1 receptor-associated kinase 1 (IRAK1) and tumor necrosis factor receptor-associated factor 6 (TRAF6) upon IL-17A treatment were analyzed, and the IL-17A-stimulated inflammation following the silencing of IRAK1 and TRAF6 was observed. In addition, the correlation between miR-146a and IL-17A in human gastric mucosa with H. pylori was examined. The results indicated that IL-17A-induced miR-146a may regulate the inflammatory response during the infection of H. pylori in a nuclear factor-B-dependent manner. Furthermore, the expression of miR-146a and IL-17A are positively correlated in human gastric mucosa infected with H. pylori. These data suggested that miR-146a may serve as a biomarker or therapeutic target in gastritis therapy.