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Effects and mechanism of Bifidobacterium on intestinal inflammation resulting from deoxycholic acid-induced M1 polarization of macrophages.

TL;DR

Bifidobacterium can inhibit HFD-induced intestinal inflammation or that resulting from DCA-induced M1 polarization of macrophages, and may regulate bile acid levels and target cholesterol metabolism pathways as potential therapeutic strategies for HFD-associated colitis.

Key Findings

High-fat diet (HFD) or deoxycholic acid (DCA) promotes infiltration of colon macrophages and their polarization toward the M1 phenotype.

  • HFD and DCA both induced macrophage recruitment and pro-inflammatory (M1) polarization in the colon
  • Polarization was assessed through real-time polymerase chain reaction and immunofluorescence staining
  • This M1 polarization was associated with intestinal inflammation in the HFD animal model

Both vancomycin and Bifidobacterium inhibited HFD- or DCA-induced M1 polarization of macrophages.

  • Vancomycin was administered to significantly reduce the population of intestinal gram-positive bacteria, thereby reducing fecal DCA levels
  • Bifidobacterium supplementation similarly inhibited M1 macrophage polarization
  • Both interventions reduced recruitment of pro-inflammatory macrophages in the HFD animal model

Bifidobacterium enhanced species richness and uniformity of intestinal microbiota in HFD mice, but this effect was not observed in the presence of vancomycin.

  • Bifidobacterium improved alpha diversity metrics (species richness and uniformity) in HFD-fed mice
  • Co-administration of vancomycin abolished Bifidobacterium's ability to improve these diversity parameters
  • Bifidobacterium did not increase the absolute abundance of microbiota in either HFD-fed or HFD-and-vancomycin-treated mice
  • Intestinal microbiota composition was assessed using 16S rRNA high-throughput sequencing

HFD altered the relative abundance of intestinal microbiota at both the phylum and genus levels, and these changes were partially mitigated by Bifidobacterium or vancomycin.

  • HFD induced shifts in microbiota composition at multiple taxonomic levels
  • Both Bifidobacterium supplementation and vancomycin treatment partially reversed HFD-induced changes in microbiota relative abundance
  • Changes were characterized using 16S rRNA high-throughput sequencing

Bifidobacterium may regulate bile acid levels and target cholesterol metabolism pathways as mechanisms underlying its anti-inflammatory effects.

  • Fecal DCA levels were measured using liquid chromatography-mass spectrometry
  • Vancomycin reduced gram-positive bacteria populations, which contributed to reduced fecal DCA levels, suggesting a microbiota-bile acid axis
  • Bifidobacterium's regulation of bile acid levels and cholesterol metabolism pathways were identified as potential therapeutic strategies for HFD-associated colitis

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Citation

Yang P, Xiao C, Wang J, Yan C, Li Q, Li S, et al.. (2026). Effects and mechanism of Bifidobacterium on intestinal inflammation resulting from deoxycholic acid-induced M1 polarization of macrophages.. World journal of gastroenterology. https://doi.org/10.3748/wjg.v32.i6.113010