Effect of Clostridium butyricum against Microglia‐Mediated Neuroinflammation in Alzheimer's Disease via Regulating Gut Microbiota and Metabolites Butyrate

Dec 14, 2019Molecular nutrition & food research

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

AI simplified

Gut-Brain Axis on OpenScience ↗PubMed ↗DOI ↗

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.

AI 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.

Full Text

Full text is available at the source.

View full text (PDF) ↗View full text (XML) ↗View full text ↗

Effect of Clostridium butyricum against Microglia‐Mediated Neuroinflammation in Alzheimer's Disease via Regulating Gut Microbiota and Metabolites Butyrate

Abstract

Full Text

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the gut-brain axis brief

Abstract

Full Text

Related papers

You found one interesting study. We’ll send the next 7.

what lands in your inbox each week:

Recent issues from the gut-brain axis brief