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<p>Chronic alcohol consumption can lead to disruption of the blood-brain barrier. The gut-brain axis may be involved in this pathological process. We investigated the gut microbiota of 30 healthy individuals and 30 alcohol use disorder (AUD) patients and found that at the genus level, AUD patients had decreased <i>Faecalibacterium</i> and increased <i>Streptococcus</i>. Liquid chromatography mass spectrometer (LC-MS/MS) revealed that 604 metabolites were upregulated and 606 were downregulated in AUD patients with cognitive impairment, compared to healthy controls. Chronic alcohol consumption led to cognitive decline in mice, with increased 20 kDa FITC-dextran leakage in the prefrontal cortex (PFC) and hippocampus, and decreased expression of ZO-1, occludin, and claudin-5. Transplantation of feces from AUD patients into germ-free mice resulted in increased 20 kDa FITC-dextran leakage in PFC and hippocampus, and decreased expression of ZO-1, occludin, and claudin-5, compared to mice receiving feces from healthy individuals. Administration of <i>Faecalibacterium prausnitzii</i> to chronically alcohol-fed mice improved cognitive function, reduced 20 kDa FITC-dextran leakage in PFC and hippocampus, and increased the expression of ZO-1, occludin, and claudin-5. Chronic alcohol consumption can disrupt the blood-brain barrier through the gut-brain axis. <i>Faecalibacterium prausnitzii</i> can improve alcohol-induced blood-brain barrier disruption and cognitive impairment.</p>

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Chronic alcohol consumption disrupts the integrity of the blood-brain barrier through the gut-brain axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月25日

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  • Chenguang Li,
  • Hongxuan Wang,
  • Xinrou Lin,
  • Guanyong Zeng,
  • Xiangpen Li,
  • Wanru Chen,
  • Hengjian Lu,
  • Jingrui Pan,
  • Xiaoni Zhang,
  • Xiaoming Rong,
  • Lei He,
  • Ying Peng

摘要

Chronic alcohol consumption can lead to disruption of the blood-brain barrier. The gut-brain axis may be involved in this pathological process. We investigated the gut microbiota of 30 healthy individuals and 30 alcohol use disorder (AUD) patients and found that at the genus level, AUD patients had decreased Faecalibacterium and increased Streptococcus. Liquid chromatography mass spectrometer (LC-MS/MS) revealed that 604 metabolites were upregulated and 606 were downregulated in AUD patients with cognitive impairment, compared to healthy controls. Chronic alcohol consumption led to cognitive decline in mice, with increased 20 kDa FITC-dextran leakage in the prefrontal cortex (PFC) and hippocampus, and decreased expression of ZO-1, occludin, and claudin-5. Transplantation of feces from AUD patients into germ-free mice resulted in increased 20 kDa FITC-dextran leakage in PFC and hippocampus, and decreased expression of ZO-1, occludin, and claudin-5, compared to mice receiving feces from healthy individuals. Administration of Faecalibacterium prausnitzii to chronically alcohol-fed mice improved cognitive function, reduced 20 kDa FITC-dextran leakage in PFC and hippocampus, and increased the expression of ZO-1, occludin, and claudin-5. Chronic alcohol consumption can disrupt the blood-brain barrier through the gut-brain axis. Faecalibacterium prausnitzii can improve alcohol-induced blood-brain barrier disruption and cognitive impairment.