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<p>Spinal cord injury (SCI) disrupts gut flora and exacerbates neuroinflammation. Evidence supports the important role of the intestinal microbiota in SCI. This study evaluated the neuroprotective effect of <i>Limosilactobacillus reuteri</i> (<i>L. reuteri</i>) DSM 17938 on SCI and its potential anti-inflammatory mechanism. The intestinal microbiota was disorganised following SCI, with a significant decrease in the abundance of probiotic bacteria such as <i>L. reuteri</i>. <i>L. reuteri</i> DSM17938 treatment improved the spinal cord pathology and enhanced locomotor functional recovery in SCI-model rats. Moreover, it modulated tryptophan metabolism by promoting indole-3-carboxaldehyde production. In addition, <i>L. reuteri</i> DSM17938 inhibits polarization of M1 microglia and reduces the production of IL-6, IL-1 β, and TNF—α in spinal cord injury to alleviate neuroinflammation. It also activates aryl hydrocarbon receptor (AhR) signalling via upregulating AhR and CYP1A1 expression, promoting tight junction protein synthesis. In summary, <i>L. reuteri</i> DSM17938 promotes SCI recovery by modulating tryptophan metabolism to activate AhR signalling and intestinal barrier repair to attenuate spinal cord M1 microglial activation and neuroinflammation, suggesting a strategy for clinical adjuvant SCI treatment.</p>

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Limosilactobacillus reuteri DSM17938 Attenuates Neuroinflammatory Responses After Spinal Cord Injury by Modulating Tryptophan Metabolism

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月26日

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  • Qiuyu Cen,
  • Yanru Cui,
  • Jing Feng,
  • Li Zhu,
  • Juanfang Wei,
  • Linjie Wang,
  • Cong Chang,
  • Rizhao Pang,
  • Junyu Wang,
  • Anren Zhang

摘要

Spinal cord injury (SCI) disrupts gut flora and exacerbates neuroinflammation. Evidence supports the important role of the intestinal microbiota in SCI. This study evaluated the neuroprotective effect of Limosilactobacillus reuteri (L. reuteri) DSM 17938 on SCI and its potential anti-inflammatory mechanism. The intestinal microbiota was disorganised following SCI, with a significant decrease in the abundance of probiotic bacteria such as L. reuteri. L. reuteri DSM17938 treatment improved the spinal cord pathology and enhanced locomotor functional recovery in SCI-model rats. Moreover, it modulated tryptophan metabolism by promoting indole-3-carboxaldehyde production. In addition, L. reuteri DSM17938 inhibits polarization of M1 microglia and reduces the production of IL-6, IL-1 β, and TNF—α in spinal cord injury to alleviate neuroinflammation. It also activates aryl hydrocarbon receptor (AhR) signalling via upregulating AhR and CYP1A1 expression, promoting tight junction protein synthesis. In summary, L. reuteri DSM17938 promotes SCI recovery by modulating tryptophan metabolism to activate AhR signalling and intestinal barrier repair to attenuate spinal cord M1 microglial activation and neuroinflammation, suggesting a strategy for clinical adjuvant SCI treatment.