Weissella cibaria SGW054 alleviates neurodegenerative progression in Proteus mirabilis- and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease mice by regulating gut microbiota dysbiosis

Aug 30, 2025Brain, behavior, and immunity

Weissella cibaria SGW054 reduces Parkinson’s disease progression in mice by improving gut bacteria imbalance caused by Proteus mirabilis and MPTP

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Abstract

Weissella cibaria SGW054 may serve as a novel therapeutic supplement for Parkinson's disease by protecting against dopaminergic neuronal loss.

SGW054 exhibited antibacterial activity against Proteus mirabilis, which is associated with Parkinson's disease pathology.
In a mouse model of Parkinson's disease induced by Proteus mirabilis, SGW054 improved motor dysfunction and reduced neurodegeneration.
SGW054 decreased microgliosis, colonic inflammatory cytokine release, and gut barrier disruption while controlling fecal Proteus mirabilis levels.
In a separate MPTP-induced Parkinson's disease mouse model, SGW054 mitigated glial hyperactivation and lowered proinflammatory cytokine release in the brain and colon.
Fecal microbiota analysis indicated that SGW054 administration alleviated microbiota dysbiosis by reducing Proteus mirabilis and increasing beneficial bacteria.

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Emerging evidence suggests that gut microbiota dysbiosis contributes to the initial stages of neuroinflammation and dopaminergic neurodegeneration in Parkinson's disease (PD). Probiotics are receiving attention as a treatment for PD because they restore gut microbiota balance and brain homeostasis. In this study, we demonstrated that Weissella cibaria SGW054 (SGW054), a probiotic strain, exhibited antibacterial activity against Proteus mirabilis (PM), which induces PD pathology. We evaluated the therapeutic effects of SGW054 on PD pathology in PM-induced PD model mice. Subsequently, we assessed the effects of SGW054 in mice exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin commonly used to induce PD, and explored its influence on gut microbiota composition. SGW054 improved motor dysfunction and neurodegeneration in PM-treated PD model mice. Additionally, SGW054 reduced microgliosis, colonic inflammatory cytokine release, gut barrier disruption, and the translocation of α-synuclein aggregates from the gut to the brain by controlling fecal PM levels. In an MPTP-induced PD mouse model, SGW054 mitigated glial hyperactivation and lowered the release of proinflammatory cytokines, such as tumor necrosis factor-α, in both the brain and colon, thereby relieving dopaminergic neuronal damage and behavioral complications. Fecal microbiota analysis demonstrated that SGW054 administration alleviated MPTP-induced microbiota dysbiosis, decreasing PM and Lachnospiraceae abundance while increasing probiotic bacteria levels (Bacteroidaceae, Bacteroides, and Faecalibacterium), which strongly correlated with the anti-inflammatory and neuroprotective effects of SGW054. Collectively, our findings indicate that SGW054 may serve as a novel therapeutic supplement for PD by protecting against dopaminergic neuronal loss, restoring inflammatory homeostasis, and correcting gut microbiota dysbiosis in both gut-initiated and brain-initiated PD subtypes.

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