Molecular nutrition & food researchDec 14, 2019

Clostridium butyricum may reduce brain inflammation in Alzheimer's by changing gut bacteria and butyrate levels

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 5, 2026

Abstract

Clostridium butyricum treatment for 4 weeks prevented cognitive impairment in APP/PS1 mice.

Cognitive testing showed improved performance in mice treated with Clostridium butyricum.
Treatment reduced amyloid-β deposits and microglial activation in the brains of transgenic mice.
Proinflammatory cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels were decreased after treatment.
Abnormal gut microbiota and butyrate levels were normalized following Clostridium butyricum treatment.
Butyrate treatment lowered markers of microglial activation, including CD11b and cyclooxygenase-2 (COX-2).
Clostridium butyricum may influence neuroinflammation through the gut-brain axis via butyrate.

Simplified

SCOPE: Recent evidences demonstrate that abnormal gut microbiota (GM) might be involved in the pathogenesis of Alzheimer's disease (AD). However, the role of probiotics in preventing AD by regulating GM-gut-brain axis remains unclear. Here, the anti-neuroinflammatory effect and its mechanism of probiotic Clostridium butyricum (CB) against AD is investigated by regulating GM-gut-brain axis.

METHODS AND RESULTS: APPswe/PS1dE9 (APP/PS1) transgenic are treated intragastrically with CB for 4 weeks then cognitively tested. Amyloid-β (Aβ) burden, microglial activation, proinflammatory cytokines production, GM, and metabolites butyrate are analyzed. Moreover, Aβ-induced BV2 microglia are pretreated with butyrate, and the levels of cluster of differentiation 11b (CD11b), cyclooxygenase-2 (COX-2), and NF-κB p65 phosphorylation are determined. The results show that CB treatment prevents cognitive impairment, Aβ deposits, microglia activation, and production of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the brain of APP/PS1 mice. Meanwhile, abnormal GM and butyrate are reversed after CB treatment. Notably, butyrate treatment reduces the levels of CD11b and COX-2, and suppresses phosphorylation of NF-κB p65 in the Aβ-induced BV2 microglia.

CONCLUSIONS: These findings indicate that CB treatment could attenuate microglia-mediated neuroinflammation via regulating the GM-gut-brain axis, which is mediated by the metabolite butyrate.

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Clostridium butyricum may reduce brain inflammation in Alzheimer's by changing gut bacteria and butyrate levels

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