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Related Concept Videos

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Related Experiment Video

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Mendelian Randomization Unlocks Stroke Therapeutics: Dioscin Inhibits CD27-Driven Neuroinflammation via Gut

Haozhou Tan1,2, Shengli Li3, Han Yan4

  • 1Clinical Laboratory, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221004, Jiangsu, China.

Molecular Neurobiology
|November 20, 2025
PubMed
Summary

Investigating the gut-brain-immune axis in ischemic stroke, this study links specific B cells (CD27+) to increased stroke risk and identifies beneficial gut bacteria (Burkholderiales) offering protection via FGF19 signaling.

Keywords:
GWASGut microbiotaImmune cellsInflammatory proteinsIschemic strokeMendelian randomization

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Area of Science:

  • Neuroscience
  • Immunology
  • Microbiome research

Background:

  • The gut-brain-immune axis is crucial in ischemic stroke, but causal links between gut dysbiosis, immune dysfunction, and cerebrovascular damage are not fully understood.
  • Understanding these connections is vital for developing novel stroke therapies.

Purpose of the Study:

  • To elucidate the causal relationships between gut microbial composition, immune system activity, and ischemic stroke risk.
  • To identify specific immune cells and microbial pathways involved in stroke pathogenesis and protection.

Main Methods:

  • Bayesian weighted Mendelian randomization (BWMR) was employed, integrating large-scale genetic data for immune traits, inflammatory proteins, gut microbes, and ischemic stroke.
  • Colocalization analysis confirmed shared genetic variants, and computational modeling explored therapeutic interventions.

Main Results:

  • Elevated CD27 protein on specific memory B cells (CD24+ CD27+ and IgD- CD38dim) was genetically associated with increased risk of large-artery atherosclerosis stroke.
  • The gut bacteria order Burkholderiales demonstrated a protective effect against small-vessel stroke, with g_Odoribacter's benefit partially mediated by FGF19 signaling.
  • Dioscin was identified as a potential therapeutic agent to inhibit CD27.

Conclusions:

  • CD27-expressing B cells are implicated as drivers of neuroinflammation in stroke.
  • Targeting CD27 with compounds like Dioscin presents a potential therapeutic strategy.
  • Gut microbes, through pathways like FGF19, offer a protective mechanism against stroke, highlighting the microbiome's role in cerebrovascular health.