瘤介导的微生物群变化会通过IL-1β生产损害海马体CA1区域的突触标记/捕获
Ying Zhu1, Yu Mei1, Nimmi Baby2
1Immunology Translational Research Programme, Department of Microbiology of Immunology, Yong Loo Lin School of Medicine, Immunology Programme, Life Sciences Institute, National University of Singapore, Singapore, 117456, Singapore.
Communications biology
|July 3, 2023
概括
肝细胞癌 (HCC) 通过改变肠道微生物群,从而影响突触可塑性,从而损害认知功能. 恢复微生物群或阻止IL-1β改善了瘤携带小鼠的认知缺陷.
科学领域:
- 神经科学是一个神经科学.
- 胃肠病学 胃肠病学
- 在瘤学瘤学.
背景情况:
- 癌症,特别是肝细胞癌 (HCC),与认知障碍有关.
- 瘤诱导的神经功能障碍的确切机制和肠道微生物群的作用尚未完全理解.
研究的目的:
- 研究HCC对认知功能和肠道微生物群的影响.
- 阐明底层机制,重点关注突触标记和捕获 (STC) 和IL-1β信号.
主要方法:
- 使用了肝细胞癌 (HCC) 的小鼠模型.
- 评估认知功能和突触可塑性 (STC).
- 通过绝育和移植操纵肠道微生物群;测量血清和海马IL-1β水平.
主要成果:
- HCC的生长改变了肠道微生物群的组成和认知功能受损.
- 在携带瘤的小鼠中,突触标记和捕获 (STC) 显著减少.
- 微生物群灭菌或移植调节了STC;HCC增加了IL-1β,其耗尽恢复了STC.
结论:
- 肠道微生物群在调解HCC诱导的认知障碍方面发挥着关键作用.
- 升高的IL-1β水平是关键机制,将肠道失调与HCC的认知缺陷联系在一起.
- 准肠道微生物群和IL-1β可能为癌症相关的认知功能障碍提供治疗策略.
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