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Updated: Jan 12, 2026

Quantitative Polymerase Chain Reaction-based Analyses of Murine Intestinal Microbiota After Oral Antibiotic Treatment
Published on: November 17, 2018
Bifidobacterium infantis modulates intestinal microecology to inhibit the spread of antimicrobial resistance
Ziyun Li1,2, Jiamin Hu3, Yingmiao Pan1
1Microbiome-X, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, China.
Insights
Bifidobacterium infantis supplementation reduced antibiotic resistance gene spread in mice by enhancing bile acids and inhibiting resistant bacteria. This probiotic intervention offers a new strategy to combat antimicrobial resistance (AMR) and protect gut health.
Area of Science:
- Microbiology and Gut Health
- Antimicrobial Resistance (AMR) Mechanisms
- Probiotic and Gut Microbiota Modulation
Background:
- Early antibiotic use in children increases susceptibility to multidrug-resistant infections.
- The role of probiotics in curbing antimicrobial resistance (AMR) and antibiotic resistance gene (ARG) spread is not fully understood.
- Gut microbiota imbalance due to antibiotic overuse elevates the risk of horizontal gene transfer of ARGs.
Purpose of the Study:
- To investigate the role of Bifidobacterium infantis in inhibiting the spread of antibiotic resistance genes (ARGs) within the gut.
- To elucidate the mechanisms by which B. infantis modulates the gut environment to reduce ARG dissemination.
- To provide a theoretical basis for novel probiotic interventions against AMR.
Main Methods:
- Supplementation of mice with Bifidobacterium infantis 15697.
- Analysis of gut microbiota composition, bile acid synthesis, and ARG abundance.
- Utilized a mouse infection model to assess the impact of B. infantis on antibiotic-resistant Escherichia coli colonization and horizontal gene transfer.
Main Results:
- B. infantis supplementation significantly increased bile acid synthesis (TUDCA, TCA) and the abundance of beneficial probiotics like Parabacteroides goldsteinii.
- B. infantis inhibited the colonization of antibiotic-resistant E. coli and reduced horizontal gene transfer events, thereby decreasing ARG spread.
- Tauroursodeoxycholic acid (TUDCA) and taurocholic acid (TCA) were found to inhibit biofilm formation and decrease cell membrane permeability in antibiotic-resistant bacteria by interacting with the OmpC protein.
Conclusions:
- Bifidobacterium infantis plays a crucial role in regulating gut microbiota and suppressing the spread of antibiotic resistance genes (ARGs).
- The mechanism involves modulation of bile acid metabolism, specifically TUDCA and TCA, which directly impede antibiotic-resistant bacteria.
- B. infantis represents a promising probiotic strategy for reducing AMR, protecting gut health in children and adults, and informing public health policies.
Abstract:
Early administration of antibiotics in children may heighten the susceptibility to multidrug-resistant bacterial infections. While probiotics are commonly employed for bacterial infection management, their nuanced advantages, particularly in curtailing the spread of antimicrobial resistance (AMR), remain unclear. This study investigated the role and mechanisms of Bifidobacterium infantis in inhibiting the spread of antibiotic resistance genes (ARGs) in the gut. We found that supplementing with B. infantis 15697 significantly enhanced the synthesis of bile acids in mouse feces, particularly tauroursodeoxycholic acid (TUDCA) and taurocholic acid (TCA). Concurrently, the abundance of potential probiotics such as Parabacteroides goldsteinii in the gut significantly increased. Using a mouse infection model, we discovered that B. infantis supplementation inhibited the colonization of antibiotic-resistant Escherichia coli in the gut and the events of horizontal gene transfer, thereby reducing the spread of ARGs. Further analysis revealed that TUDCA and TCA, through their interaction with the OmpC protein, decreased the biofilm formation capability and cell membrane permeability of antibiotic-resistant bacteria, inhibiting the horizontal spread of ARGs. These findings reveal the important role of B. infantis in regulating the gut microbiota and inhibiting the spread of ARGs, providing a theoretical basis for developing new probiotic intervention strategies. This could help reduce the global spread of AMR and protect human health.
Importance:
The global spread of antimicrobial resistance (AMR) has become a significant threat to public health, particularly in children, where the overuse of antibiotics leads to gut microbiota imbalance and increases the risk of horizontal transfer of antibiotic resistance genes (ARGs). This study supplemented mice with Bifidobacterium infantis 15697, which significantly enhanced the synthesis of bile acids, especially tauroursodeoxycholic acid and taurocholic acid, while promoting the growth of probiotics and inhibiting the colonization of antibiotic-resistant bacteria and the spread of ARGs. This finding not only reveals the important role of B. infantis in regulating the gut microbiota and inhibiting the spread of ARGs but also provides a theoretical basis for developing new probiotic intervention strategies. By modulating the gut microbiota and bile acid metabolism, B. infantis has the potential to become an effective means of reducing the spread of AMR. This is of great significance for protecting the gut health of children and adults, reducing the risk of resistant infections, and also provides scientific evidence for the formulation of global public health policies.
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