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Xenosiderophore Utilization Promotes Bacteroides thetaiotaomicron Resilience during Colitis.
异种铁载体利用促进结肠炎期间的拟杆菌属 thetaiotaomicron 恢复力。
- 影响因子:10.50
- DOI:10.1016/j.chom.2020.01.010
- 作者列表:"Zhu W","Winter MG","Spiga L","Hughes ER","Chanin R","Mulgaonkar A","Pennington J","Maas M","Behrendt CL","Kim J","Sun X","Beiting DP","Hooper LV","Winter SE
- 发表时间:2020-02-11
Abstract
:During short-lived perturbations, such as inflammation, the gut microbiota exhibits resilience and reverts to its original configuration. Although microbial access to the micronutrient iron is decreased during colitis, pathogens can scavenge iron by using siderophores. How commensal bacteria acquire iron during gut inflammation is incompletely understood. Curiously, the human commensal Bacteroides thetaiotaomicron does not produce siderophores but grows under iron-limiting conditions using enterobacterial siderophores. Using RNA-seq, we identify B. thetaiotaomicron genes that were upregulated during Salmonella-induced gut inflammation and were predicted to be involved in iron uptake. Mutants in the xusABC locus (BT2063-2065) were defective for xenosiderophore-mediated iron uptake in vitro. In the normal mouse gut, the XusABC system was dispensable, while a xusA mutant colonized poorly during colitis. This work identifies xenosiderophore utilization as a critical mechanism for B. thetaiotaomicron to sustain colonization during inflammation and suggests a mechanism of how interphylum iron metabolism contributes to gut microbiota resilience.
摘要
: 在短暂的扰动过程中,如炎症,肠道菌群表现出弹性并恢复到原来的构型。虽然在结肠炎过程中微生物对微量营养素铁的获取减少,但病原体可以通过使用铁载体清除铁。共生细菌如何在肠道炎症过程中获得铁尚不完全清楚。奇怪的是,人类共生拟杆菌 thetiotaomicron 不产生铁载体,而是在使用肠杆菌铁载体的铁限制条件下生长。使用 RNA-seq,我们鉴定了在沙门氏菌诱导的肠道炎症过程中上调并预测参与铁摄取的 B.Thetaiotomicron 基因。XusABC 位点 (BT2063-2065) 的突变体在体外对异种铁载体介导的铁摄取有缺陷。在正常小鼠肠道中,XusABC 系统是可有可无的,而一个 xusA 突变体在结肠炎期间定植不良。这项工作确定了异种铁载体的利用是 B.Thetaiotomicron 在炎症期间维持定植的关键机制,并提出了门间铁代谢如何促进肠道菌群恢复的机制。
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