Yang PC, Xiao CY, Wang J, Yan CH, Li QY, Li SY, Li J, Zhang LJ, Dai CB. Effects and mechanism of Bifidobacterium on intestinal inflammation resulting from deoxycholic acid-induced M1 polarization of macrophages. World J Gastroenterol 2026; 32(6): 113010 [DOI: 10.3748/wjg.v32.i6.113010]
Corresponding Author of This Article
Chi-Bing Dai, Professor, Department of Gastroenterology, Affiliated Renhe Hospital of China Three Gorges University, No. 435 Yiling Road, Yichang 443001, Hubei Province, China. dchibing@126.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Feb 14, 2026 (publication date) through Feb 5, 2026
Times Cited of This Article
Times Cited (0)
Journal Information of This Article
Publication Name
World Journal of Gastroenterology
ISSN
1007-9327
Publisher of This Article
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Share the Article
Yang PC, Xiao CY, Wang J, Yan CH, Li QY, Li SY, Li J, Zhang LJ, Dai CB. Effects and mechanism of Bifidobacterium on intestinal inflammation resulting from deoxycholic acid-induced M1 polarization of macrophages. World J Gastroenterol 2026; 32(6): 113010 [DOI: 10.3748/wjg.v32.i6.113010]
Peng-Chun Yang, Jing Wang, Cai-Hua Yan, Qi-Yi Li, Shi-Yu Li, Jian Li, Li-Jing Zhang, Chi-Bing Dai, Department of Gastroenterology, Affiliated Renhe Hospital of China Three Gorges University, Yichang 443001, Hubei Province, China
Chun-Yan Xiao, Department of Oncology, Yilin People’s Hospital of Yichang City, Yichang 443099, Hubei Province, China
Co-first authors: Peng-Chun Yang and Chun-Yan Xiao.
Author contributions: Yang PC and Xiao CY performed most of the experiment and data analysis, wrote the manuscript, and contributed equally as co-first authors; Li QY, Wang J, and Yan CH provided experiment assistance; Li SY, Li J, and Zhang LJ contributed to interpretation of the data and analyses; Dai CB provided experimental design and guidance. All of the authors have read and approved the manuscript.
Supported by Scientific Research Project of Hubei Provincial Health Commission, No. WJ2021F060; and the Open Fund of the Basic and Clinical Pathology Research Center of Three Gorges University, No. RHKFBL2022-13.
Institutional animal care and use committee statement: This study was approved by the Institutional Animal Care and Use Committee of China Three Gorges University.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: The datasets generated and analyzed during the present study are available from the corresponding author on reasonable request.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Chi-Bing Dai, Professor, Department of Gastroenterology, Affiliated Renhe Hospital of China Three Gorges University, No. 435 Yiling Road, Yichang 443001, Hubei Province, China. dchibing@126.com
Received: August 13, 2025 Revised: October 23, 2025 Accepted: December 11, 2025 Published online: February 14, 2026 Processing time: 173 Days and 23.7 Hours
Abstract
BACKGROUND
A high-fat diet (HFD) can cause systemic low-grade inflammation, metabolic and inflammatory diseases, and alter the composition of intestinal microbiota. Although probiotics mitigate intestinal inflammation, it is still unclear whether they can directly inhibit the production of deoxycholic acid (DCA) to prevent or alleviate intestinal inflammation.
AIM
To investigate changes in intestinal flora, fecal DCA levels, and cytokine profiles.
METHODS
Vancomycin was administered to significantly reduce the population of intestinal gram-positive bacteria, which helped in reducing the fecal DCA levels. Recruitment of pro-inflammatory macrophages, polarization of macrophages, and the inflammation associated with the intestinal flora of the HFD animal model were assessed. Their expression levels were analyzed through real-time polymerase chain reaction, immunofluorescence staining, liquid chromatography-mass spectrometry, and 16S rRNA high-throughput sequencing.
RESULTS
HFD or DCA promotes the infiltration of colon macrophages, causing their polarization toward the M1 phenotype. This polarization can be inhibited by both vancomycin and Bifidobacterium. Bifidobacterium enhances the species richness and uniformity of the intestinal microbiota in HFD mice; however, it does not improve these parameters in the presence of vancomycin. Bifidobacterium also does not increase the abundance of microbiota in HFD-fed or HFD-and-vancomycin-treated mice. HFD alters the relative abundance of intestinal microbiota at the phylum and genus levels. Bifidobacterium or vancomycin can partially mitigate these changes.
CONCLUSION
Bifidobacterium can inhibit HFD-induced intestinal inflammation or that resulting from DCA-induced M1 polarization of macrophages. It may also regulate bile acid levels and target cholesterol metabolism pathways, which may serve as potential therapeutic strategies for HFD-associated colitis.
Core Tip: A high-fat diet increases fecal deoxycholic acid (DCA), inducing M1 macrophage polarization and intestinal inflammation. Bifidobacterium mitigates this by reducing the production of DCA, inhibiting M1 polarization, and partially restoring gut microbiota balance. Hence, they can be employed for treating high-fat diet-associated colitis. This study aims to investigate changes in intestinal flora, fecal DCA levels, and cytokine profiles.
