ACE2将氨基酸营养不良与微生物生态和肠道炎症联系起来
Tatsuo Hashimoto1, Thomas Perlot, Ateequr Rehman
1IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, 1030 Vienna, Austria.
Nature
|July 28, 2012
概括
ангиотензин I 转化酶 2 (Ace2) 缺乏症通过破坏氨基酸平衡和肠道微生物群,增加对肠道炎症的易感性. 这就解释了营养不良如何导致肠道问题.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
背景情况:
- 营养不良影响全球超过10亿人,经常导致腹和肠道炎症.
- 连接饮食失衡与肠道功能障碍的确切机制尚不清楚.
- 氨酸- ангиотензин系统 (RAS) 酶,氨酸I转化酶2 (Ace2),在各种生理过程中至关重要.
研究的目的:
- 研究Ace2在维持肠道平衡中的作用及其与营养不良引起的炎症的联系.
- 阐明Ace2通过哪些机制影响肠道免疫力,微生物组成和对结肠炎的易感性.
主要方法:
- 研究了Ace2缺乏的小鼠,以评估对化学诱导的上皮损伤和大肠炎的敏感性.
- 分析了肠道氨基酸平衡的变化,抗微生物的表达和肠道微生物群的组成.
- 从Ace2突变小鼠进行便微生物群移植到无菌野生型接受者.
- 研究了饮食中托对Ace2依赖性肠道调节的影响.
主要成果:
- 缺乏Ace2显著增加了对肠道炎症和结肠炎的敏感性.
- Ace2调节肠道氨基酸平衡,抗微生物的表达和肠道微生物生态,独立于RAS.
- 在Ace2突变小鼠中改变的肠道微生物群传递了对无菌宿主增加的结肠炎易感性.
- 饮食中的托直接影响Ace2介导的肠道免疫和微生物群的调节.
结论:
- Ace2是饮食氨基酸平衡,天生的免疫力和肠道微生物组成的关键调节者.
- 缺少Ace2导致感染性结肠炎的易感性,为营养不良相关的肠道炎症提供了分子基础.
- 准Ace2介导途径可能为营养不良相关的胃肠道疾病提供治疗策略.
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