维生素B12促进了肠道失调和炎症微环境,增强了Tet2缺乏的血液形成
bioRxiv : the preprint server for biology
|September 5, 2025
概括
高维生素B12水平可能会通过破坏肠道细菌和减少有益的短链脂肪酸 (SCFA) 来恶化克隆造血. 补充SCFA如黄酸可以逆转这些效应,这表明了CH的新疗法.
科学领域:
- 血液学
- 微生物学
- 癌症学
背景情况:
- 血清维生素B12水平升高与克隆造血 (CH) 和骨髓性恶性瘤风险增加有关.
- 维生素B12的补充会影响肠道微生物群和短链脂肪酸 (SCFA) 的产生,这对肠道健康至关重要.
- TET2突变驱动CH,可能受到微生物信号和维生素B12的影响.
研究的目的:
- 在一个缺乏Tet2的CH模型中研究维生素B12补充的微环境影响.
- 探索肠道微生物组在维生素B12对CH进展的影响中的作用.
主要方法:
- 在Tet2缺乏和野生类型小鼠模型中评估B12补充的效果.
- 骨髓形成的分析,骨髓细胞对细菌刺激的反应,以及炎症性细胞因子水平.
- 评估肠道微生物组成和产生SCFA的细菌,使用黄酸盐进行干预.
主要成果:
- 维生素B12补充增强了骨髓形成和骨髓细胞对细菌刺激的反应.
- 在补充B12后观察到循环炎性细胞因子的增加.
- 维生素B12诱导肠道失调并减少SCFA产生细菌,但酸盐可以逆转效应.
结论:
- 维生素B12可以通过肠道微生物组破坏SCFA代谢来促进CH的进展.
- 补充SCFA,特别是黄糖酸,显示出缓解CH的治疗策略.
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