• Qihui Zhou, Fengtian Wu, Shiwei Chen, Panpan Cen, Qin Yang, Jun Guan, Li Cen, Tianbao Zhang, Haihong Zhu, and Zhi Chen.
• Department of Infectious Diseases, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China; Department of Infectious Diseases, Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
• Nutrition. 2022 Jul 1; 99-100: 111673.

ObjectivesWe aimed to explore whether Lactobacillus reuteri could have a positive role in reducing inflammation and bacterial translocation in rats with acute liver failure.MethodsLactobacillus reuteri were gavaged to Sprague-Dawley (SD) rats at a dose of 1 × 109 CFU/mL once a day for 14 d. D-galactosamine was injected intraperitoneally to induce acute liver failure for 24 h on the 15th day. Liver function, liver and ileum histology, intestinal cytokines, intestinal tight junction proteins, lipopolysaccharide binding protein, apoptosis molecules, and nuclear factor erythroid-derived 2 (Nrf-2) / heme oxygenase (HO-1) molecules were assessed.ResultsThe results showed that L. reuteri alleviated liver injury and intestinal inflammation induced by D-galactosamine. L. reuteri also improved the expression of intestinal tight junction proteins and maintained the integrity of the intestinal barrier by inhibiting apoptosis of intestinal epithelial cells. L reuteri induced an increase in Nrf-2 nuclear translocation and elevated induction of HO-1. L. reuteri treatment significantly enhanced the expression of phosphoinositide 3-kinase/protein kinase B (PI3 K/Akt), protein kinase C (PKC), and their phosphorylated forms but not mitogen-activated protein kinase. The nuclear factor kappa B (NF-κB) pathway was inhibited after L. reuteri treatment. Interleukin (IL)-17A produced by Th17 cells and γδT17 cells may not contribute to an improved function of the intestinal barrier in L. reuteri-treated SD rats.ConclusionsOverall, our study indicated that L. reuteri-induced expression of intestinal tight junction proteins is mediated by the PI3 K/Akt-Nrf-2/HO-1-NF-κB and PKC-Nrf-2/HO-1-NF-κB pathways, which leads to inhibition of the apoptosis of intestinal epithelial cells, thus maintaining the integrity of the damaged intestinal barrier.Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

20 keywords...

hide…