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来自细菌的非正规聚胺对抗宿主线粒体功能

Kelsie M Nauta¹, Darrick R Gates¹, Matthew Weiland¹

¹Van Andel Research Institute, Department of Metabolism and Nutritional Programing, Grand Rapids, MI, USA.

Nature communications

|November 26, 2025

概括

肠道细菌可以产生一种新型的多胺,N1-aminopropylagmatine (N1-APA),它破坏肠道细胞功能,并可能通过影响线粒体应激反应,导致炎症性肠道疾病.

科学领域:

微生物学微生物学
分子生物学分子生物学
毒理学毒理学毒理学

背景情况:

肠道细菌聚胺与肠道细胞相互作用,可能影响炎症性肠道疾病 (IBD).
关联肠道微生物组聚胺代谢与IBD病变的分子机制在很大程度上仍未被定义.

研究的目的:

通过使用模型生物体,研究微生物组衍生的多氨酸的生物活性.
在肠道细胞中阐明聚胺中间体N1-aminopropylagmatine (N1-APA) 的分子机制.

主要方法:

使用基于衍生性的液态色谱-质谱法 (LC-MS).
采用了模型生物Caenorhabditis elegans和小鼠骨髓巨细胞.
通过CATP-5传送器进行研究的聚胺运输.

主要成果:

确定了N1-aminopropylagmatine (N1-APA) 作为由大肠杆菌和细菌细菌产生的一种非正规的聚胺中间体.
在C. elegans中表现出N1-APA生物活性,对抗发育并激活线粒体展开的蛋白质反应.
显示的N1-APA抑制了eIF5A的低化和替代性巨细胞激活,类似于脱氧基素合成酶抑制剂.

结论:

细菌N1-APA是一种具有潜在作用于线粒体应激反应的生物活性代谢物.
异常的肠道微生物组聚胺代谢,导致N1-APA的产生,可能有助于IBD的发病.
需要进一步的研究来确定N1-APA的所有点及其在疾病中的确切作用.

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