Bacillus coagulans TCI803 Confers Gastroesophageal Protection against Helicobacter pylori-Evoked Gastric Oxidative Stress and Acid-Induced Lower Esophageal Sphincter Inflammation

Abstract

Probiotic Bacillus coagulans TCI803 (BC) may have impact on gastrointestinal protection. This study was designed to investigate the effects of BC on Helicobacter pylori (H. pylori) induced gastric inflammation in mice and acid-induced lower esophageal sphincter (LES) dysfunction in rat. We determined the oxidative stress/apoptosis/autophagy signaling pathway in H. pylori-induced gastric inflammation and HCl-evoked LES inflammation. H. pylori increased leukocyte infiltration mediated inflammation and gastric cytokines array, 3NT/4HNE-mediated oxidative stress and Bax/Caspase 3-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. Esophageal infusion of saline evoked an increase of LES pressure and efferent vagus nerve activity during the emptying phase, however, esophageal infusion of HCl dysregulated LES motility 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. In summary, we suggest that 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.