饮食与微生物组的相互作用促进了脊髓损伤后肠道神经系统的弹性
Adam M Hamilton1, Lisa Blackmer-Raynolds1, Yaqing Li1
1Department of Cell Biology, Emory University School of Medicine, Atlanta GA 30329.
bioRxiv : the preprint server for biology
|June 19, 2024
概括
食胰岛素通过调节肠道微生物及其代谢物来预防脊髓损伤 (SCI) 后的肠道神经系统缩和肠道动力障碍. 这突出了神经性肠道治疗的饮食-微生物群-免疫轴.
科学领域:
- 神经科学是一个神经科学.
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 脊髓损伤 (SCI) 导致广泛的生理功能障碍,包括肠道动力障碍和肠道神经系统 (ENS) 缩.
- 尽管ENS具有典型的弹性,但SCI后持续性肠道问题的确切原因仍然不清楚.
- 新兴的研究将SCI与肠道微生物组的改变联系在一起,这表明SCI在ENS恢复中可能发挥作用.
研究的目的:
- 调查调节肠道微生物组是否可以促进SCI后的ENS恢复.
- 确定食纤维 (胰岛素) 和微生物代谢物对肠道功能和SCI后ENS完整性的影响.
主要方法:
- 患有SCI的小鼠被用胰岛素,SCI相关的微生物组或微生物短链脂肪酸 (SCFA) 治疗.
- 评估了对ENS缩,肠道不运动以及IL-10信号传递的作用的影响.
主要成果:
- 在SCI小鼠中,注射胰岛素预防了ENS缩,并减少了肠道动力障碍.
- 仅仅微生物干预并没有完全恢复肠道功能.
- 微生物衍生的SCFA模仿了胰岛素对ENS的保护作用.
- 胰岛素的保护作用取决于细胞因子IL-10的信号传递.
结论:
- 饮食干预措施,特别是胰岛素,可以保护ENS,并改善SCI后的肠功能.
- 微生物代谢物 (SCFA) 在这种保护作用中起着至关重要的作用.
- 涉及IL-10的饮食-微生物群-免疫轴对SCI后的ENS弹性至关重要.
- 这个轴为SCI诱导的神经性肠道提供了潜在的治疗点.
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