Helicobacterpylori infection impairs gastric epithelial barrier function via microRNA‑100‑mediated mTOR signaling inhibition.

Abstract

Helicobacterpylori (H.pylori) infection has an important effect on human health as it is an established cause of gastric carcinoma. microRNAs (miRNAs/miRs) are a family of small RNAs with various functions in the control of cellular profiles. However, the effect of miR‑100 in H.pylori infection remains unknown. Healthy volunteers (n=100) and patients with H.pylori infection (n=98) were included in the present study. H.pylori infection was confirmed by urea breath tests. The levels of miR‑100 in gastroscopic biopsy samples and cultured GES‑1 cells were measured by reverse transcription‑quantitative polymerase chain reaction. Furthermore, miR‑100 was overexpressed or inhibited in GES‑1 cells by an miR‑100 mimic or inhibitor, respectively. The expression of cell‑junction proteins and members of the mechanistic target of rapamycin kinase (mTOR) signaling pathway was investigated by western blotting. The results demonstrated that miR‑100 levels were upregulated in infected patients and cultured gastric epithelial cells, compared with the respective controls. Additionally, the expression of epithelial (E)‑cadherin and zona occludens‑1 in the gastric mucosa of infected patients and GES‑1 cells was downregulated. Furthermore, infected gastric epithelial cells exhibited impaired barrier functions, as measured by resistance and permeability tests. Overexpression of miR‑100 inhibited junction protein expression, as well as the activation of the mTOR signaling pathway, while suppression of miR‑100 restored E‑cadherin expression and mTOR signaling. The results of the present study indicate that H.pylori infection may cause dysfunction of the gastric epithelial barrier by increasing miR‑100 levels, which subsequently inhibit mTOR signaling. These results may have potential applications affecting miR‑100 in H.pylori‑related diseases.