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细菌为何能破坏宿主细胞的抑制剂

摘要 : 德国弗赖堡大学的研究人员发现,细菌对宿主细胞产生毒性所需的一类重要基因被发现可以用于编码一类酶,而该类酶能够让从哺乳动物身上获取的抑制剂发生转变从而不再对抗食物中的这些细菌,这是《自然—化学生物学》上在线发表的一项研究得出的结论。

德国弗赖堡大学的研究人员发现,细菌对宿主细胞产生毒性所需的一类重要基因被发现可以用于编码一类酶,而该类酶能够让从哺乳动物身上获取的抑制剂发生转变从而不再对抗食物中的这些细菌,这是《自然—化学生物学》上在线发表的一项研究得出的结论。

最近研究显示,某些能够产生化合物亚甲基丁二酸的哺乳动物细胞能够对细菌感染产生反应。亚甲基丁二酸可以抑制细菌代谢中的一种中心酶,防止细菌生长并帮助清除感染。人们已经弄清细菌在不利的宿主环境中的几种存活机制,但其如何阻止亚甲基丁二酸的抑制效果却是未知。

Ivan Berg等人检测到细菌体内一组对细菌毒性起重要作用的基因能够编码一种酶,这种酶可以将宿主细胞中的亚甲基丁二酸降解成单一单元结构。反过来,这些单元结构又能用于细菌细胞的生长以及细菌正常的代谢过程。研究人员报告称,这些基因存在于许多细菌包括非致病性种类中,这表明其能在各种环境中为细菌提供一个选择性优势。

原文摘要:

Bacterial itaconate degradation promotes pathogenicity

Jahminy Sasikaran, Michał Ziemski, Piotr K Zadora, Angela Fleig & Ivan A Berg

Itaconate (methylenesuccinate) was recently identified as a mammalian me-tabolite whose production is substantially induced during macrophage activation. This compound is a potent inhibitor of isocitrate lyase, a key enzyme of the glyoxylate cycle, which is a pathway required for the survival of many pathogens inside the eukaryotic host. Here we show that numerous bacteria, notably many pathogens such as Yersinia pestis and Pseudomonas aeruginosa, have three genes for itaconate degradation. They encode itaconate coenzyme A (CoA) transferase, itaconyl-CoA hydratase and (S)-citramalyl-CoA lyase, formerly referred to as CitE-like protein. These genes are known to be crucial for survival of some pathogens in macrophages. The corresponding enzymes convert itaconate into the cellular building blocks pyruvate and acetyl-CoA, thus enabling the bacteria to me-tabolize itaconate and survive in macrophages. The itaconate degradation and detoxification pathways of Yersinia and Pseudomonas are the result of convergent evolution. This work revealed a common persistence factor operating in many pathogenic bacteria.

来源: Nature中文 浏览次数:216

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