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Fucose sensing regulates bacterial intestinal colonization

机译：岩藻糖感测调节细菌肠道定植

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摘要

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 theta-iotaomicron produces multiple fucosidases that cleave fucose from host glycans, resulting in high fucose availability in the gut lumen6. 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.
机译：哺乳动物的胃肠道为微生物群提供了复杂而竞争的环境。病原体成功定居需要清除营养，感应化学信号，与常驻细菌竞争并精确调节毒力基因的表达。胃肠道病原体肠出血性大肠杆菌（EHEC）依赖于王国间的化学传感系统来调节毒力基因的表达。在这里，我们显示这些系统控制名为FusKR的新型两组分信号转导系统的表达，其中FusK是组氨酸传感器激酶，而FusR是响应调节剂。 FusK感知岩藻糖并控制毒力和代谢基因的表达。这种岩藻糖感测系统是哺乳动物肠道强劲EHEC定植所必需的。岩藻糖在肠中含量很高。拟杆菌β-iotaomicron产生多种岩藻糖苷酶，可从宿主聚糖上裂解岩藻糖，从而导致肠道内腔中岩藻糖的利用率较高。在粘蛋白中生长期间，thetaiotaomicron可以通过从粘蛋白中裂解岩藻糖来增强EHEC的毒力，从而激活FusKR信号级联，调节EHEC的毒力基因表达。我们的发现表明，EHEC使用岩藻糖（一种由微生物群提供的宿主来源的信号）来调节EHEC的致病性和新陈代谢。

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  • 来源
    《Nature》 |2012年第7427期|113-117|共5页
  • 作者

    Alline R. Pacheco; Meredith M. Curtis; Jennifer M. Ritchie; Diana Munera; Matthew K. Waldor; Cristiano G. Moreira; Vanessa Sperandio;

  • 作者单位

    Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9048, USA,Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas,Texas 75390-9048, USA;

    Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9048, USA,Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas,Texas 75390-9048, USA;

    Division of Infections Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA;

    Division of Infections Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA;

    Division of Infections Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA;

    Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9048, USA,Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas,Texas 75390-9048, USA;

    Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9048, USA,Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas,Texas 75390-9048, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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