Cen Qiuyu, Cui Yanru, Feng Jing, Zhu Li, Wei Juanfang, Wang Linjie, Chang Cong, Pang Rizhao, Wang Junyu, Zhang Anren
Department of Rehabilitation Medicine, Shanghai Fourth People's Hospital Affiliated to Tongji University, Shanghai, 200080, China.
School of Health Preservation and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu, 610036, China.
Probiotics Antimicrob Proteins. 2025 Apr 26. doi: 10.1007/s12602-025-10545-y.
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.
脊髓损伤（SCI）会破坏肠道菌群并加剧神经炎症。有证据支持肠道微生物群在脊髓损伤中发挥的重要作用。本研究评估了罗伊氏乳杆菌（L. reuteri）DSM 17938对脊髓损伤的神经保护作用及其潜在的抗炎机制。脊髓损伤后肠道微生物群紊乱，罗伊氏乳杆菌等益生菌的丰度显著降低。罗伊氏乳杆菌DSM17938治疗改善了脊髓损伤模型大鼠的脊髓病理学状况并增强了运动功能恢复。此外，它通过促进吲哚 - 3 - 甲醛的产生来调节色氨酸代谢。此外，罗伊氏乳杆菌DSM17938抑制脊髓损伤中M1小胶质细胞的极化并减少白细胞介素 - 6、白细胞介素 - 1β和肿瘤坏死因子 - α的产生，以减轻神经炎症。它还通过上调芳烃受体（AhR）和细胞色素P450 1A1（CYP1A1）的表达来激活芳烃受体信号通路，促进紧密连接蛋白的合成。总之，罗伊氏乳杆菌DSM17938通过调节色氨酸代谢来激活芳烃受体信号通路以及修复肠道屏障，从而减轻脊髓M1小胶质细胞的激活和神经炎症，促进脊髓损伤的恢复，为脊髓损伤临床辅助治疗提供了一种策略。
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