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Background <p>The microbiota-gut-brain axis plays a pivotal role in numerous neurological disorders, including traumatic brain injury (TBI). TBI induces neuroinflammation accompanied by alterations in the gut microbiota. However, the contribution of gut microbiota dysbiosis to post-TBI neuroinflammation and its underlying mechanisms remain poorly understood.</p> Results <p>Here, we found that TBI mice treated with Akkermansia(Akk) exhibited increased Akkermansia abundance at 28 days post-TBI, whereas those receiving fecal microbiota transplantation (FMT) showed elevated levels of Bifidobacteriaceae and Bifidobacterium. Both Akk and FMT alleviated persistent microglial activation in the hippocampus of TBI mice at 28 days. FMT prevented the reduction of 5-hydroxyindole in TBI mice, and prolonged FMT suppressed the sphingolipid signaling pathway in these animals. Furthermore, two macrophage activation-associated genes, ACx3cr1 and Cd68, were upregulated after TBI, but their expression was inhibited by FMT at 28 days. Sphingolipid metabolism was elevated in TBI mice at 7 and 28 days post-injury, and Akk treatment (<i>p</i> = 0.027) effectively blocked this increase at 28 days.</p> Conclusion <p>This study suggests that prolonged Akkermansia supplementation may mitigate post-TBI microglial activation by modulating the sphingolipid metabolic pathway. Both FMT and Akk represent potential therapeutic targets for developing novel strategies to address persistent microglial activation and chronic neuroinflammation following TBI, though their precise mechanisms require further validation.</p>

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Multi-omics characterized the effects of Akkermansia muciniphila and fecal microbiota transplant on the microglial activation after traumatic brain injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月30日

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  • Shuai Wang,
  • Xuemei Fan,
  • Zhipeng Zheng,
  • Qiao Gu,
  • Shurui Xu,
  • Ying Zhu,
  • Fangjie Zhang,
  • Mengyuan Diao,
  • Wei Hu

摘要

Background

The microbiota-gut-brain axis plays a pivotal role in numerous neurological disorders, including traumatic brain injury (TBI). TBI induces neuroinflammation accompanied by alterations in the gut microbiota. However, the contribution of gut microbiota dysbiosis to post-TBI neuroinflammation and its underlying mechanisms remain poorly understood.

Results

Here, we found that TBI mice treated with Akkermansia(Akk) exhibited increased Akkermansia abundance at 28 days post-TBI, whereas those receiving fecal microbiota transplantation (FMT) showed elevated levels of Bifidobacteriaceae and Bifidobacterium. Both Akk and FMT alleviated persistent microglial activation in the hippocampus of TBI mice at 28 days. FMT prevented the reduction of 5-hydroxyindole in TBI mice, and prolonged FMT suppressed the sphingolipid signaling pathway in these animals. Furthermore, two macrophage activation-associated genes, ACx3cr1 and Cd68, were upregulated after TBI, but their expression was inhibited by FMT at 28 days. Sphingolipid metabolism was elevated in TBI mice at 7 and 28 days post-injury, and Akk treatment (p = 0.027) effectively blocked this increase at 28 days.

Conclusion

This study suggests that prolonged Akkermansia supplementation may mitigate post-TBI microglial activation by modulating the sphingolipid metabolic pathway. Both FMT and Akk represent potential therapeutic targets for developing novel strategies to address persistent microglial activation and chronic neuroinflammation following TBI, though their precise mechanisms require further validation.