脊髓损伤引起的神经性肠道:宿主微生物群相互作用在肠道疼痛和功能障碍中的作用
Adam B Willits1, Leena Kader1, Olivia Eller2
1Department of Anesthesiology, Pain and Perioperative Medicine, University of Kansas Medical Center, Kansas City, KS, United States.
脊髓损伤 (SCI) 通过增加结肠素基因相关 (CGRP) 来引起神经性肠道 (NB),导致肠道失调和疼痛. 这项研究确定了开发新NB治疗的关键机制.
科学领域:
- 神经科学是一个神经科学.
- 胃肠病学 胃肠病学
- 再生医学是一种再生医学.
背景情况:
- 脊髓损伤 (SCI) 影响数百万人,其中60%的人患有神经性肠道 (NB),其特点是便秘和疼痛.
- 目前的NB干预是以症状为重点的,并且由于对潜在机制的知识差距,在很大程度上无效.
- 这项研究旨在阐明启动和维持SCI后NB的机制,以开发新疗法.
研究的目的:
- 确定驱动神经性肠道 (NB) 后脊髓损伤 (SCI) 的机制.
- 为NB开发基于证据的治疗策略.
- 了解CGRP和肠道微生物组在SCI引起的肠道功能障碍中的作用.
主要方法:
- 在动物中使用T9脊柱伤模型.
- 采用了全转录组分析 (RNAseq),16SrRNA测序和Ca2+成像.
- 结合组织学,分子和功能评估来分析肠道变化.
主要成果:
- SCI诱导了结肠中素基因相关 (CGRP) 表达的增加,这表明神经性炎症.
- 观察到结肠传输时间增加,结构损伤和粘液层破坏.
- 检测到肠道微生物组失生症,随着Anaeroplasma的增加,以及高响应的阴道 afferents和肠道神经元.
结论:
- SCI导致结肠CGRP过度表达,改变肠道结构和功能.
- 神经性炎症和肠道失调有助于SCI后内脏疼痛敏感化.
- 这些发现为预防SCI患者的NB发展提供了潜在的治疗点.
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