nature20121206-6

来自美国德州大学科研人员揭示了岩藻糖在肠道细菌定植中的作用机制。

-2012年12月6日《自然》

中文翻译


【题目】岩藻糖传感调控细菌肠道定植

【译文】哺乳动物的胃肠道为菌群提供了一个复杂和竞争激烈的环境。成功定植的病原体,需要清除的营养物质,检测化学信号,与细菌竞争和精确调节的毒力基因的表达。 胃肠道病原体肠出血性大肠杆菌(EHEC)依赖于领域内的化学传感系统调节毒力基因表达。本研究表明这些系统控制着表达一种新型的双组分信号转导系统,名为FusKR,FusK是组氨酸传感器激酶,而FusR则是反应调节器。 FusK感知岩藻糖并控制毒力基因及能量代谢相关基因的表达。哺乳动物肠道中大量肠出血性大肠杆菌需要岩藻糖的传感系统。在肠道内,岩藻糖极为丰富,多形拟杆菌产生大量岩藻糖酶,将宿主中聚糖裂解为岩藻糖,致使肠腔中出现高浓度岩藻糖供应量。在粘蛋白生长过程中,B.thetaiotaomicron切割粘蛋白中的岩藻糖,有助于肠出血性大肠杆菌的毒力从而激活FusKR的信号级联,调节肠出血性大肠杆菌的毒力基因表达。我们的发现表明岩藻糖利用微生物产生的宿主衍生信号调节肠出血性大肠杆菌的致病及代谢。

英文原稿


[Title]: Fucose sensing regulates bacterial intestinal colonization

[Authors]:Alline R. Pacheco,1, 2 Meredith M. Curtis,1, 2 Jennifer M. Ritchie,3 Diana Munera,3 Matthew K. Waldor,3 Cristiano G. Moreira1, 2 & Vanessa Sperandio1, 2

[Abstract]The mammalian gastrointestinal tract provides a complex and competitive environment for the microbiota. Successful colonization by pathogens requires scavenging nutrients, sensing chemical signals, competing with the resident bacteria and precisely regulating the expression of virulence genes. The gastrointestinal pathogen enterohaemorrhagic Escherichia coli (EHEC) relies on inter-kingdom chemical sensing systems to regulate virulence gene expression. Here we show that these systems control the expression of a novel two-component signal transduction system, named FusKR, where FusK is the histidine sensor kinase and FusR the response regulator. FusK senses fucose and controls expression of virulence and metabolic genes. This fucose-sensing system is required for robust EHEC colonization of the mammalian intestine. Fucose is highly abundant in the intestine. Bacteroides thetaiotaomicron produces multiple fucosidases that cleave fucose from host glycans, resulting in high fucose availability in the gut lumen. During growth in mucin, B. thetaiotaomicron contributes to EHEC virulence by cleaving fucose from mucin, thereby activating the FusKR signalling cascade, modulating the virulence gene expression of EHEC. Our findings suggest that EHEC uses fucose, a host-derived signal made available by the microbiota, to modulate EHEC pathogenicity and metabolism.

原文地址

http://www.nature.com/nature/journal/v492/n7427/full/nature11623.html

 

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