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Updated: Aug 29, 2025
Quantitative Polymerase Chain Reaction-based Analyses of Murine Intestinal Microbiota After Oral Antibiotic Treatment
Published on: November 17, 2018
Antibiotics-induced depression in mice via the microbiota-gut-brain axis
Xingli Fan1, Handan Deng1, Jianing Qiu1
1Departments of Basic Medicine and Forensic Medicine, Hangzhou Medical College, Hangzhou, Zhejiang 310053, PR China.
Background:
Intestinal dysbacteriosis is associated with depression. This study aimed to establish an antibiotics-induced depression mouse model and explore the mechanism of antibiotic-induced depression.
Methods:
C57BL/6 J mice were treated with antibiotics to prepare the antibiotic-induced depression mouse model. Behavioral tests and depression-related bio-markers were examined. To understand the abundance of different bacteria in intestinal flora and screen out the predominant bacterial species, metagenomic analysis of feces was carried out. Finally, we detected the expression of NF-κB-p65 and p-NF-κB-p65 in PFC and the hippocampus using Western blot.
Results:
Mixtures A and B caused depression-like behavior in mice. Norepinephrine, 5-hydroxytryptamine, and brain-derived neurotrophic factor in hippocampus and PFC of antibiotic-induced depression mice significantly decreased. The serum adrenocorticotropic hormone and corticosterone concentrations increased. The abundance values of Bacteroides thetaiotaomicron, Klebsiella oxytoca, and Klebsiella aerogenes in antibiotic-induced depression mice significantly increased, and the characteristic KO genes and metabolic pathways in antibiotic-induced depression mice were significantly different with in CUMS depression mice (the positive control) and normal mice. The relative levels of p-NF-κB-p65 in antibiotics-induced depression mice were significantly higher than in normal mice.
Limitations:
How dysbacteriosis induces inflammation in the central nervous system is unclear.
Conclusions:
Specific antibiotic mixture can cause depression-like behavior and changes of depression-related bio-markers in mice. The antibiotic-induced depression mice display changes in the species and metabolism of intestinal bacterial flora. The activation of NF-κB inflammatory signaling pathway in the central nervous system may act as one of the mechanisms in the development of antibiotic-induced depression.
Insights
Antibiotics can induce depression-like behaviors in mice by altering gut bacteria and activating the NF-κB inflammatory pathway in the brain. This study establishes an antibiotic-induced depression model to explore these mechanisms.
Area of Science:
- Neuroscience
- Microbiology
- Pharmacology
Background:
- Intestinal dysbacteriosis is increasingly linked to the development of depression.
- Understanding the mechanisms connecting gut health and mental well-being is crucial.
Purpose of the Study:
- To establish a mouse model of antibiotic-induced depression.
- To investigate the underlying mechanisms, including changes in gut microbiota and central nervous system inflammation.
Main Methods:
- C57BL/6J mice were treated with antibiotics to induce depression-like behaviors.
- Behavioral tests, biochemical analyses of depression-related biomarkers, fecal metagenomic sequencing, and Western blot analysis of NF-κB signaling in the brain were performed.
Main Results:
- Antibiotic treatment induced depression-like behaviors and altered levels of key neurotransmitters and hormones.
- Metagenomic analysis revealed significant changes in the abundance and metabolic pathways of gut bacteria, including increases in Bacteroides thetaiotaomicron, Klebsiella oxytoca, and Klebsiella aerogenes.
- Increased levels of phosphorylated NF-κB p65 (p-NF-κB-p65) were observed in the prefrontal cortex and hippocampus, indicating activation of the NF-κB inflammatory pathway.
Conclusions:
- Specific antibiotic mixtures can induce depression-like phenotypes in mice.
- Antibiotic-induced depression is associated with significant alterations in gut microbiota composition and function.
- Activation of the NF-κB inflammatory signaling pathway in the central nervous system is implicated as a key mechanism in the development of antibiotic-induced depression.
