Bacillus coagulans TCI803 confers gastroesophageal protection against Helicobacter pylori -evoked gastric oxidative stress and acid-induced lower esophageal sphincter inflammation.

Abstract

Background: Probiotic Bacillus coagulans (BC) may have an impact on gastrointestinal protection. This study was designed to investigate the BC effects on Helicobacter pylori ( H. pylori ) induced gastric inflammation in mice and acid-induced lower esophageal sphincter (LES) dysfunction in rats. We determined the oxidative stress/apoptosis/autophagy signaling pathways in H. pylori -induced gastric inflammation and HCl-evoked LES inflammation.

Methods: H. pylori -induced gastric inflammation was used in 40 mice and HCl-evoked LES inflammation in 40 Wistar rats. Western blot, immunohistochemistry and cytokine array were used to determine the pathophysiologic mechanisms.

Results: H. pylori increased leukocyte infiltration-mediated inflammation and the expression levels of gastric cytokines, 3NT/4HNE-mediated oxidative stress, and Bax/Caspase3-mediated apoptosis, but decreased Beclin-1/LC3-II-mediated autophagy in the mice gastric mucosa. BC treatment decreased inflammation, cytokines release, oxidative stress, and apoptosis, and reversed autophagy in H. pylori -infected gastric mucosa. To replace the antibiotic therapy, BC TCI803 was selected to inhibit H. pylori infection for commercial interests. Saline esophageal infusion evoked an increase in LES pressure and efferent vagus nerve activity during the emptying phase. However, HCI dysregulated LES motility esophageal infusion by a decrease in threshold pressure, intercontraction interval and an increase in efferent vagus nerve activity. BC treatment significantly recovered the level of threshold pressure, intercontraction interval, and depressed the enhanced efferent vagus nerve activity. In vitro LES wire myography data displayed that HCl-treated LES significantly decreased the contractile response to acetylcholine. BC treatment significantly restored the contractile response to acetylcholine in LES wire myography. LES after HCl stimulation significantly increased leukocyte infiltration-mediated inflammation, whereas BC treatment effectively reduced the leukocyte infiltration-mediated inflammation in the HCl-treated LES.

Conclusion: BC via anti-oxidation and anti-inflammation confers gastroesophageal protection against H. pylori involved oxidative stress/inflammation/apoptosis/autophagy signaling in mice with gastric inflammation and HCl-induced LES dysregulation and inflammation.