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Related Experiment Videos

Xiaowei Sun1, Zhenhui Chen2, Lu Yu3

  • 1Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Institute of Gastroenterology of Guangdong Province, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Frontiers in Pharmacology
|June 9, 2023
PubMed
Summary

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This summary is machine-generated.

The probiotic Bacteroides dorei BDX-01 alleviates acute colitis by enhancing bile acid metabolism and regulating the FXR-NLRP3 pathway. This study highlights BDX-01 as a potential treatment for ulcerative colitis.

Area of Science:

  • Microbiology
  • Gastroenterology
  • Immunology

Background:

  • Intestinal dysbiosis and altered bile acid (BA) metabolism are linked to ulcerative colitis (UC) pathogenesis.
  • The specific mechanisms by which bacterial strains modulate BA metabolism to treat colitis remain unclear.
  • This study investigates the effects of Bacteroides dorei BDX-01 on acute colitis and its underlying mechanisms.

Purpose of the Study:

  • To evaluate the safety and efficacy of the novel probiotic strain Bacteroides dorei BDX-01 in a mouse model of acute colitis.
  • To elucidate the mechanisms by which BDX-01 ameliorates colitis, focusing on bile acid metabolism and inflammatory pathways.
  • To determine the role of gut microbiota in the protective effects of BDX-01.

Main Methods:

  • Safety assessment of BDX-01 in vitro and in vivo.
Keywords:
Bacteroidesbile acidbile salt hydrolasefarnesoid X receptorinflammasomeprobioticulcerative colitis

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  • Induction of acute colitis in mice using dextran sulfate sodium (DSS).
  • Evaluation of BDX-01's anti-inflammatory effects using cell lines and molecular techniques (qPCR, Western blotting).
  • Analysis of gut microbiota composition (16S rRNA sequencing), fecal bile salt hydrolase (BSH) activity, and BA profiles (targeted metabolomics).
  • Investigation using antibiotic-treated pseudo-germ-free mice and in vitro assays.

    • Main Results:

    • BDX-01 was confirmed safe and significantly reduced symptoms and pathology in DSS-induced acute colitis.
    • BDX-01 treatment increased intestinal BSH activity and BA deconjugation, altering specific BA ratios and deoxycholic acid levels.
    • BDX-01 upregulated colonic farnesoid X receptor (FXR) and fibroblast growth factor 15 (FGF15), while downregulating key inflammatory mediators (NLRP3, ASC, cleaved caspase-1, IL-1β).
    • The protective effect of BDX-01 was independent of major gut microbiota alterations and TβMCA abolished its effects on FXR and NLRP3 inflammasome activation.

    Conclusions:

    • Bacteroides dorei BDX-01 effectively ameliorates DSS-induced acute colitis.
    • The therapeutic effects are mediated by the regulation of intestinal BSH activity and the FXR-NLRP3 signaling pathway.
    • BDX-01 represents a promising probiotic strategy for managing ulcerative colitis.