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Updated: Oct 27, 2025
A Method to Assess Bacteriocin Effects on the Gut Microbiota of Mice
Published on: July 25, 2017
Stachyose inhibits vancomycin-resistant Enterococcus colonization and affects gut microbiota in mice
Siyi Zhu1, Xianping Li2, Liqiong Song2
1State Key Laboratory for Infectious Disease Prevention and Control, National Institute for Communicable Disease Control and Prevention, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Chinese Center for Disease Control and Prevention, Changping, Research Units of Discovery of Unknown Bacteria and Function (2018 RU010), Chinese Academy of Medical Sciences, Beijing, 102206, PR China; Shunyi Maternal and Children's Hospital of Beijing Children's Hospital, PR China.
Stachyose supplementation effectively reduces vancomycin-resistant Enterococcus (VRE) colonization in mice by altering gut microbiota composition. This dietary intervention also promotes beneficial bacteria and influences host gene expression, offering a potential strategy against VRE infections.
Area of Science:
- Microbiology
- Gastroenterology
- Immunology
Background:
- Nosocomial infections caused by vancomycin-resistant Enterococcus (VRE) are a growing global health concern.
- Dietary interventions targeting gut microbiota modulation are being explored as a strategy to combat VRE infections.
- Stachyose, a prebiotic, shows potential for promoting probiotic growth and inhibiting VRE.
Purpose of the Study:
- To determine if stachyose inhibits VRE colonization in a mouse model.
- To investigate the role of gut microbiota in mediating stachyose's effect on VRE.
Main Methods:
- VRE-infected and uninfected mice received oral stachyose or PBS for 7 days.
- VRE colonization was assessed by cultivation.
- Gut microbiota composition was analyzed using 16S rRNA sequencing, and gene expression was evaluated via RNA-sequencing.
Main Results:
- Stachyose significantly reduced VRE colonization in infected mice.
- Stachyose altered gut microbiota, increasing Porphyromonadaceae and Parabacteroides in infected mice, and Lactobacillus in uninfected mice.
- Stachyose modulated host gene expression, including TNF and IL-17 signaling pathways in infected mice, and metabolic pathways in uninfected mice.
Conclusions:
- Stachyose supplementation effectively inhibits VRE colonization, likely through modulation of gut microbiota composition.
- Stachyose influences host gene expression, suggesting a broader impact on host physiology.
- Stachyose may offer health benefits in normal mice by increasing Lactobacillus abundance and upregulating metabolic pathways.
