World journal of gastroenterology · 2026
Effects and mechanism of Bifidobacterium on intestinal inflammation resulting from deoxycholic acid-induced M1 polarization of macrophages.
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Yang Peng-Chun, Xiao Chun-Yan, Wang Jing, Yan Cai-Hua, Li Qi-Yi, Li Shi-Yu, Li Jian, Zhang Li-Jing, Dai Chi-Bing
Аннотация
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 Bifidoba cterium. 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.
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 Bifidoba cterium. 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.