Orally Administered Bacillus licheniformis F0726 Attenuates MPTP/P-Induced Neurodegeneration by Modulating Gut
Wenqian Wang1,2,3, Xinni Wu1,2,3, Kuo Meng1,2,3
1Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, Tianjin 300457, P. R. China.
Abstract:
Extensive studies have shown that Parkinson's disease (PD) is associated with disruption in the gut microbiota. Bacillus licheniformis has attracted the attention of researchers due to its function in regulating the composition of intestinal microbiota. This study investigated the neuroprotective effects of orally administered B. licheniformis F0726 in an MPTP/P-induced mice model of PD. The results showed that B. licheniformis F0726 significantly alleviated MPTP/P-induced motor dysfunction and depletion of dopamine-containing neurons. Notably, B. licheniformis F0726 alleviated neuroinflammation by inhibiting glial cell activation and reducing serum pro-inflammatory cytokine levels. Furthermore, 16S rRNA sequencing revealed that intervention with B. licheniformis F0726 alleviated the gut dysbiosis. Crucially, B. licheniformis F0726 significantly increased the level of short-chain fatty acids, which are key signaling molecules of the gut-brain axis. In conclusion, B. licheniformis F0726 may alleviate neurodegenerative lesions in PD mice by modulating the gut microbiota and suppressing inflammatory responses.
Insights
Bacillus licheniformis F0726 shows neuroprotective effects in Parkinson's disease (PD) models. This probiotic alleviates motor dysfunction, neuroinflammation, and gut dysbiosis by modulating microbiota and increasing beneficial short-chain fatty acids.
Area of Science:
- Neuroscience
- Microbiology
- Immunology
Background:
- Parkinson's disease (PD) is linked to gut microbiota alterations.
- Bacillus licheniformis influences intestinal microbiota composition.
Purpose of the Study:
- Investigate the neuroprotective potential of B. licheniformis F0726 in a mouse model of PD.
- Evaluate its effects on motor function, neuronal health, neuroinflammation, and gut microbiota.
Main Methods:
- MPTP/P-induced mouse model of Parkinson's disease.
- Oral administration of B. licheniformis F0726.
- Behavioral tests for motor function.
- Measurement of dopamine-containing neurons.
- Assessment of glial cell activation and pro-inflammatory cytokines.
- 16S rRNA sequencing for gut microbiota analysis.
- Quantification of short-chain fatty acids.
Main Results:
- B. licheniformis F0726 significantly improved motor function and protected dopamine-producing neurons.
- It reduced neuroinflammation by inhibiting glial activation and lowering pro-inflammatory cytokines.
- Gut dysbiosis was alleviated, with increased levels of short-chain fatty acids.
Conclusions:
- B. licheniformis F0726 demonstrates neuroprotective effects in a PD mouse model.
- It acts by modulating gut microbiota, suppressing inflammation, and enhancing short-chain fatty acid production.
- This highlights the gut-brain axis as a therapeutic target for Parkinson's disease.
