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Gut Microbiota-Derived Butyrate Strengthens Blood-Brain Barrier Integrity and Attenuates Streptococcus suis

Wangyuan Yao1, Meili Chen1, Huachun Pan2

  • 1College of Veterinary Medicine, Southwest University, Chongqing 400010, China, swu.edu.cn.

Transboundary and Emerging Diseases
|August 18, 2026
PubMed

Insights

Sodium butyrate (NaB) protects against Streptococcus suis serotype 2 (SS2) infection by restoring gut microbiota, maintaining blood-brain barrier integrity, and reducing neuroinflammation via Nrf2 activation. This highlights the gut-brain axis as a therapeutic target for zoonotic CNS infections.

Area of Science:

  • Neuroscience
  • Microbiology
  • Immunology

Background:

  • Streptococcus suis serotype 2 (SS2) causes severe meningitis and mortality in humans and swine.
  • The gut-brain axis and its metabolites play a role in regulating neuroinflammation.
  • Understanding how gut metabolites impact SS2-induced neuroinflammation is crucial.

Purpose of the Study:

  • To investigate the protective effects of sodium butyrate (NaB) against SS2 infection in a mouse model.
  • To elucidate the mechanisms underlying NaB's neuroprotective effects, focusing on the gut-brain axis, blood-brain barrier integrity, and neuroinflammation.
  • To assess the role of Nrf2 signaling in NaB's therapeutic actions.

Main Methods:

  • Oral administration of NaB to SS2-infected mice.
  • Assessment of mortality, neuropathological signs, bacterial loads, and blood-brain barrier (BBB) integrity.
  • 16S rRNA sequencing to analyze gut microbiota composition.
  • Western blotting and ELISA to measure protein expression and cytokine levels in brain tissue and cell cultures.
  • Pharmacological inhibition of Nrf2 to determine its role in NaB's effects.

Main Results:

  • NaB administration significantly reduced mortality and neuropathological signs in SS2-infected mice.
  • Butyrate treatment preserved BBB integrity, reduced bacterial load in the brain, and restored gut microbiota homeostasis.
  • NaB upregulated Nrf2 and its antioxidant effectors while inhibiting NF-κB signaling and pro-inflammatory cytokine production.
  • The protective effects of NaB were dependent on Nrf2 activation.

Conclusions:

  • Sodium butyrate demonstrates significant prophylactic potential against SS2-induced neuroinflammation and mortality.
  • Modulating the gut-brain axis through NaB supplementation can restore gut microbiota balance and protect the BBB.
  • Nrf2 signaling is a critical mediator of butyrate's anti-neuroinflammatory and antioxidant effects.
  • Targeting the gut-brain axis offers a promising therapeutic strategy for central nervous system infections caused by foodborne pathogens.
Keywords:
Nrf2/NF-κBStreptococcus suis serotype 2blood-brain barrierbutyrategut-brain axisshort-chain fatty acids

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