结肠生成是一种微生物群调节的过程,有助于血,并保护小鼠免受大肠炎的影响
Kevin Bass1, Sathish Sivaprakasam1, Gunadharini Dharmalingam-Nandagopal1
1Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, U.S.A.
The Biochemical journal
|February 19, 2024
概括
结肠中的生成,由HMGCS2介导,可以防止肠道炎症. 这一途径受到肠道微生物群的影响,在小鼠中表现出性别依赖的效应.
科学领域:
- 代谢途径 代谢途径
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 生成主要发生在肝脏中,在葡萄糖代谢受损时提供替代能源.
- 3-基-3-甲基氨基-CoA合成酶-2 (HMGCS2) 是线粒体基因生成中的速度限制酶.
- 克罗恩病和性结肠炎患者的结肠组织中观察到减少HMGCS2的表达.
研究的目的:
- 在小鼠中研究结肠生成的表达和功能.
- 确定结肠生成在实验性结肠炎和肠道屏障功能中的作用.
- 探索肠道微生物群对HMGCS2的调节.
主要方法:
- 在肠道中产生了缺乏HMGCS2的条件淘汰小鼠.
- 鼠标接受了禁食和实验性结肠炎模型.
- 分析了肠道屏障完整性,炎症标志物 (IL-6,IL-1β,TNF-α) 和结肠上皮细胞转录组.
- 使用无细菌和接受抗生素治疗的小鼠来评估微生物群的影响.
主要成果:
- 结肠生成有助于循环水平.
- 结肠中HMGCS2的删除导致了肠道屏障的破坏,并增加了对结肠炎的易感性,特别是在雄性小鼠中.
- HMGCS2的表达受到结肠微生物群的调节.
- 结肠生成对于线粒体功能,胆固醇稳态和紧密结节组织至关重要.
结论:
- 结肠中的生成在保护小鼠免受结肠炎症方面发挥着至关重要的,取决于性别的作用.
- 结肠类生成的破坏会损害肠道屏障的完整性,并加剧炎症反应.
- 结肠微生物群显著影响结肠中HMGCS2的表达.
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