Probiotics alleviate autoimmune hepatitis in mice through modulation of gut microbiota and intestinal permeability

J Nutr Biochem. 2021 Dec:98:108863. doi: 10.1016/j.jnutbio.2021.108863. Epub 2021 Sep 11.

Abstract

Autoimmune hepatitis (AIH) is an immune-mediated type of chronic liver inflammation accompanied by intestinal flora imbalance. Probiotics have been reported to ameliorate imbalances in the intestinal flora. This study aimed to investigate the effects of compound probiotic in the AIH mouse model. AIH mice were gavaged with compound probiotic and injected intraperitoneally with dexamethasone (dex) for 42 days. The results showed that these treatments suppressed hepatic inflammatory cell infiltration, serum transaminase, and Th1 and Th17 cells. However, Treg cells were increased only in the probiotics group, which indicates an immunomodulatory role of the compound probiotic. The compound probiotic maintained intestinal barrier integrity, blocked lipopolysaccharide (LPS) translocation, and inhibited the activation of the TLR4/NF-κB pathway and the production of inflammatory factors in the liver and ileum. Moreover, the compound probiotic treatment increased the abundance of beneficial bacteria and reduced the abundance of potentially harmful bacteria in gut. Compound probiotic may improve ileal barrier function while increasing the diversity of the intestinal flora, blocking the translocation of gut-derived LPS to the liver and therefore preventing activation of the TLR4/NF-κB pathway. The resulting inhibition of pro-inflammatory factor production facilitates AIH remission.

Keywords: Autoimmune hepatitis; Compound probiotic; Inflammatory; Intestinal flora; Intestinal permeability.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bifidobacterium
  • Cytokines / metabolism
  • Feces / microbiology
  • Gastrointestinal Microbiome / drug effects*
  • Hepatitis, Autoimmune / drug therapy*
  • Hepatitis, Autoimmune / metabolism
  • Ileum / metabolism
  • Inflammation / metabolism
  • Intestinal Mucosa / metabolism*
  • Lactobacillus
  • Lipopolysaccharides / metabolism
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / metabolism
  • Permeability / drug effects
  • Probiotics / pharmacology*
  • Toll-Like Receptor 4 / metabolism

Substances

  • Cytokines
  • Lipopolysaccharides
  • NF-kappa B
  • Toll-Like Receptor 4