突发性巨细胞积累损害了中枢动脉中血管周神经功能,有炎症性肠病
Elizabeth A Grunz1, Benjamin W Jones1, Olubodun Michael Lateef1
1Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO, United States.
Frontiers in physiology
|June 21, 2023
概括
炎症性肠病中的巨细胞会损害周周神经的功能,减少血液流动. 耗尽这些巨细胞可以恢复神经正常功能和中腔动脉的血管扩张.
科学领域:
- 神经免疫学 神经免疫学
- 胃肠病学 胃肠病学
- 心血管科学 心血管科学
背景情况:
- 炎症性肠病 (IBD) 涉及免疫失调,心血管风险和肠道血液流量的改变.
- 周血管神经功能对于调节血液流动至关重要,已知在IBD中受损.
- 在IBD中神经功能受损的确切机制在很大程度上是未知的.
研究的目的:
- 在炎症性肠道疾病的背景下,研究周脉神经功能受损的潜在机制.
- 阐明神经免疫相互作用在IBD期间调解血管功能障碍中的作用.
主要方法:
- 从IL10-/-与诱导IBD的小鼠与对照对中腔动脉的RNA测序.
- 在控制和IBD小鼠中使用clodronate脂质体的巨细胞枯竭.
- 通过压力肌图和电场刺激来评估周脉神经功能.
- 免疫标记用于分析白细胞群,周围神经和神经递质受体.
主要成果:
- IBD诱导了巨关联基因表达和偶然巨积累的显著增加.
- 偶然性巨细胞的枯竭逆转了与IBD相关的感觉血管扩张和交感血管收缩的缺陷.
- 乙胆介导的扩张在IBD中受损,但在巨细胞耗尽后恢复;感官扩张仍然独立于氧化.
结论:
- 偶然性巨细胞和周围神经之间的神经免疫信号传递有助于IBD中血管扩张受损.
- 准偶然性巨细胞是一个潜在的治疗策略,以维持IBD患者的肠道血液流动.
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