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ORIGINAL RESEARCH article

Front. Med.
Sec. Gastroenterology
Volume 12 - 2025 | doi: 10.3389/fmed.2025.1496023
This article is part of the Research Topic Bifidobacteria: Exploring the Roles of These Microbiome Guardians and Their Effects on Human Health View all 8 articles

Studies on the Alleviating Effect of Bifidobacterium Lactis V9 on Dextran Sodium Sulfate-Induced Colitis in Mice

Provisionally accepted
Xiaoyan Duan Xiaoyan Duan 1,2,3,4*Rilige Wu Rilige Wu 4*Jianbo Li Jianbo Li 5,6*Zeya Li Zeya Li 4*Yanqi Liu Yanqi Liu 4*Ping Chen Ping Chen 4*Bangmao Wang Bangmao Wang 1,2,3*
  • 1 Department of Gastroenterology, General Hospital, Tianjin Medical University, Tianjin, China
  • 2 Tianjin Institute of Digestive Diseases, Tianjin, China
  • 3 Tianjin Key Laboratory of Digestive Diseases, Tianjin, China
  • 4 Department of Gastroenterology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China
  • 5 Department of Nuclear Medicine, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China
  • 6 Inner Mongolia Key Laboratory of Molecular Imaging, Hohhot, China

The final, formatted version of the article will be published soon.

    Background: Inflammatory bowel disease (IBD) has become a global public health problem with complex pathogenesis and limited therapeutic options. We aimed to investigate the potential mechanisms by which Bifidobacterium lactis V9 (V9) alleviated colitis in a dextran sodium sulfateinduced colitis model mice.Methods: Mice were induced to develop colitis by drinking DSS solution to induce colitis. The expression of the relevant factors in the blood supernatant of the mice was determined by ELISA. RT-qPCR and Western blotting were used to detect mRNA and protein expression of target genes. The fecal microbiota was analyzed by 16S rRNA sequencing. Intestinal metabolites were analyzed by untargeted metabolomics;Results: V9 effectively improved the overall symptoms of the colitis model mice. H&E showed that V9 re-stored the intestinal tissue structure. ELISA showed that V9 decreased the levels of IL-6, IL-22 and TNF-α and increased IL-10, SP, VIP and 5-HT. V9 increased the expression of AHR, CYP1A1, MUC2, Claudin-3, Occludin and ZO-1, and decreased 5-hydroxytryptamine transporter and Claudin-2. V9 increased the abundance of gut microbiota in colitis mice to promote the growth of beneficial bacteria. V9 increased tryptophan metabolites, and short-chain fatty acids, and im-proved gut inflammation.Conclusions: V9 attenuates intestinal inflammation, improves the mucosal barrier, modulates intestinal microecology and exerts a protective effect in a mouse model of DSS-induced colitis.

    Keywords: Bifidobacterium lactis V9, ulcerative colitis, intestinal barrier, intestinal flora, tryptophan metabolism

    Received: 13 Sep 2024; Accepted: 09 Jan 2025.

    Copyright: © 2025 Duan, Wu, Li, Li, Liu, Chen and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Xiaoyan Duan, Department of Gastroenterology, General Hospital, Tianjin Medical University, Tianjin, China
    Rilige Wu, Department of Gastroenterology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China
    Jianbo Li, Department of Nuclear Medicine, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China
    Zeya Li, Department of Gastroenterology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China
    Yanqi Liu, Department of Gastroenterology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China
    Ping Chen, Department of Gastroenterology, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China
    Bangmao Wang, Department of Gastroenterology, General Hospital, Tianjin Medical University, Tianjin, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.