Investigating Helicobacter pylori-related pyloric hypomotility: functional, histological, and molecular alterations

Abstract

Multiple theories have been proposed describing the pathogenic mechanisms of Helicobacter pylori (H. pylori)-associated gastric motility disorders. We assessed ex-vivo pyloric activity in h.pylori infected rats, and tried to explore the associated ghrelin hormone alteration and pyloric fibrogenesis. In addition, miR-1 was assessed in pyloric tissue samples, being recently accused of having a role in smooth muscle dysfunction. Ninety adult male Wistar albino rats were assigned into 9 groups: 1)Control group, 2)Sterile broth (vehicle group), 3)amoxicillin control, 4) omeperazole control, 5)clarithromycin control, 6)triple therapy control, 7)H. pylori- group, 8)H. pylori-clarithromycin group, and 9)H.pylori-triple therapy group. Urease enzyme activity was applied as an indicator of H. pylori infection. Ex-vivo pyloric contractility was evaluated. Serum ghrelin was assessed, and histological tissue evaluation was performed. Besides, pyloric muscle miR-1 expression was measured. The immunological epithelial to mesenchymal transition (EMT) markers; transforming growth factor β (TGFβ), alpha-smooth muscle actin (α-SMA) and E-cadherin-3 were also evaluated. By H. pylori infection, a significant (P<0.001) reduced pyloric contractility index was recorded. The miR-1 expression was decreased (P<0.001) in the H. pylori-infected group, associated with reduced serum ghrelin, elevated TGFβ, and α-SMA levels and reduced E-cadherin levels. Decreased miR-1 and disturbed molecular pattern were improved by treatment. In conclusion: H. pylori infection was associated with reduced miR-1, epithelial to mesenchymal transition, and pyloric hypomotility. The miR-1 may be a target for further studies to assess its possible involvement in H.pylori associated pyloric dysfunction, which might help in management of human H. pylori manifestations and complications.