追踪NAD代谢揭示了大肠炎期间宿主和微生物组之间的适应性协调
Abrar I Alsaadi1, Lina Welz2,3, Anant A Pothakamury1
1Department of Biochemistry and Molecular Biology, The Huck Institute of Life Sciences, Pennsylvania State University, University Park, Pennsylvania, USA.
炎症性肠病 (IBD) 破坏了尼古丁胺胺腺因二核酸 (NAD+) 的平衡. 这项研究揭示了宿主和微生物代谢如何在结肠炎期间适应NAD+生产,突出了维持平衡的复杂相互作用.
科学领域:
- 微生物学 微生物学
- 代谢途径 代谢途径
- 宿主-微生物相互作用
背景情况:
- 尼古丁胺氨酸二核酸 (NAD+) 恒温的破坏与炎症性肠病 (IBD) 有关.
- 在IBD中NAD+失调的确切机制,无论是通过生产还是消费,仍然不清楚.
- 了解这些机制对于开发IBD的向疗法至关重要.
研究的目的:
- 在小鼠模型中研究酸 (DSS) 诱导的大肠炎期间的组织和光特定的NAD+代谢.
- 在炎症性压力下阐明宿主和微生物对NAD+恒温的贡献.
- 为了确定IBD中NAD+失调是否是由于产量受损,消费增加或两者兼而有之.
主要方法:
- 利用多种omics方法和稳定的同位素标记的NAD+前体.
- 在DSS诱导的大肠炎的小鼠模型中,通过静脉输液给药前体.
- 绘制了特定于组织和光层的NAD+代谢途径.
主要成果:
- 在急性结肠炎期间观察到NAD+代谢的组织特异性重新连接.
- 通过救援途径证明了增加的流量,弥补了从托减少的de novoNAD+合成.
- 发现微生物de novo NAD+生产升高,表明合作性宿主-微生物群反应.
结论:
- 主体和微生物新陈代谢在炎症性压力期间动态相互作用,以维持NAD+平衡.
- 急性结肠炎诱导了在宿主和微生物群中对NAD+生物合成途径的差异调节.
- 这些发现提供了关于IBD病变发生过程中复杂的代谢相互作用的见解.
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