Orally Administered Bacillus licheniformis F0726 Attenuates MPTP/P-Induced Neurodegeneration by Modulating Gut Microbiota and Suppressing Inflammatory Responses.

B. licheniformis F0726 significantly alleviated MPTP/P-induced motor dysfunction in a mouse model of Parkinson's disease.

• The study used an MPTP/P (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid)-induced mouse model of PD.
• Motor dysfunction was assessed behaviorally, and B. licheniformis F0726 oral administration resulted in significant attenuation of motor deficits.
• The intervention was administered orally, consistent with a gut-brain axis mechanism of action.

B. licheniformis F0726 attenuated the depletion of dopamine-containing neurons in MPTP/P-treated mice.

• MPTP/P treatment caused depletion of dopaminergic neurons, a hallmark of Parkinson's disease pathology.
• Oral administration of B. licheniformis F0726 significantly reduced this neuronal depletion.
• This neuroprotective effect was observed in the context of a subacute MPTP/P mouse model.

B. licheniformis F0726 alleviated neuroinflammation by inhibiting glial cell activation and reducing serum pro-inflammatory cytokine levels.

• Glial cell activation, a marker of neuroinflammation, was inhibited following B. licheniformis F0726 treatment.
• Serum levels of pro-inflammatory cytokines were significantly reduced in the B. licheniformis F0726-treated groups.
• Suppression of inflammatory responses was identified as a key mechanism underlying the neuroprotective effects.

16S rRNA sequencing revealed that B. licheniformis F0726 intervention alleviated MPTP/P-induced gut dysbiosis.

• Gut microbiota composition was analyzed using 16S rRNA gene sequencing.
• MPTP/P treatment caused disruption in gut microbiota composition (dysbiosis).
• B. licheniformis F0726 administration restored gut microbiota balance, suggesting modulation of the gut-brain axis.

B. licheniformis F0726 significantly increased the levels of short-chain fatty acids (SCFAs) in MPTP/P-treated mice.

• SCFAs are described as 'key signaling molecules of the gut-brain axis.'
• MPTP/P-induced PD mice showed altered SCFA levels, which were restored by B. licheniformis F0726 treatment.
• Increased SCFA levels were identified as a crucial mechanism by which B. licheniformis F0726 may exert neuroprotective effects through the gut-brain axis.