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Diet-derived galacturonic acid regulates virulence and intestinal colonization in enterohaemorrhagic Escherichia coli and Citrobacter rodentium.
Nature Microbiology ( IF 20.5 ) Pub Date : 2019-12-23 , DOI: 10.1038/s41564-019-0641-0 Angel G Jimenez 1, 2 , Melissa Ellermann 1, 2 , Wade Abbott 3, 4 , Vanessa Sperandio 1, 2
Nature Microbiology ( IF 20.5 ) Pub Date : 2019-12-23 , DOI: 10.1038/s41564-019-0641-0 Angel G Jimenez 1, 2 , Melissa Ellermann 1, 2 , Wade Abbott 3, 4 , Vanessa Sperandio 1, 2
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Enteric pathogens sense the complex chemistry within the gastrointestinal tract to efficiently compete with the resident microbiota and establish a colonization niche. Here, we show that enterohaemorrhagic Escherichia coli and Citrobacter rodentium, its surrogate in a mouse infection model, sense galacturonic acid to initiate a multi-layered program towards successful mammalian infection. Galacturonic acid utilization as a carbon source aids the initial pathogen expansion. The main source of galacturonic acid is dietary pectin, which is converted to galacturonic acid by the prominent member of the microbiota, Bacteroides thetaiotamicron. This is regulated by the ExuR transcription factor. However, galacturonic acid is also sensed as a signal through ExuR to modulate the expression of the genes encoding a molecular syringe known as a type III secretion system, leading to infectious colitis and inflammation. Galacturonic acid acts as both a nutrient and a signal directing the exquisite microbiota-pathogen relationships within the gastrointestinal tract. This work highlights that differential dietary sugar availability influences the relationship between the microbiota and enteric pathogens, as well as disease outcomes.
中文翻译：
饮食来源的半乳糖醛酸调节肠出血性大肠杆菌和啮齿类柠檬酸杆菌中的毒力和肠道菌落。
肠病原体感觉到胃肠道内的复杂化学反应，可以有效地与微生物群落竞争并建立定居环境。在这里，我们显示肠出血性大肠杆菌和啮齿类柠檬酸杆菌（其在小鼠感染模型中的替代物）感知半乳糖醛酸，以启动朝向成功的哺乳动物感染的多层程序。半乳糖醛酸用作碳源有助于最初的病原体扩展。半乳糖醛酸的主要来源是饮食中的果胶，它是由微生物群落的主要成员，拟杆菌（Bacteroides thetaiotamicron）转化为半乳糖醛酸。这由ExuR转录因子调节。然而，半乳糖醛酸还通过ExuR被感知为信号，以调节编码称为III型分泌系统的分子注射器的基因的表达，从而导致感染性结肠炎和炎症。半乳糖醛酸既是营养物，又是指示胃肠道内微生物与病原菌关系的信号。这项工作强调，饮食中糖的可利用性差异会影响微生物群和肠道病原体之间的关系，以及疾病的后果。
更新日期：2019-12-23
中文翻译：
饮食来源的半乳糖醛酸调节肠出血性大肠杆菌和啮齿类柠檬酸杆菌中的毒力和肠道菌落。
肠病原体感觉到胃肠道内的复杂化学反应，可以有效地与微生物群落竞争并建立定居环境。在这里，我们显示肠出血性大肠杆菌和啮齿类柠檬酸杆菌（其在小鼠感染模型中的替代物）感知半乳糖醛酸，以启动朝向成功的哺乳动物感染的多层程序。半乳糖醛酸用作碳源有助于最初的病原体扩展。半乳糖醛酸的主要来源是饮食中的果胶，它是由微生物群落的主要成员，拟杆菌（Bacteroides thetaiotamicron）转化为半乳糖醛酸。这由ExuR转录因子调节。然而，半乳糖醛酸还通过ExuR被感知为信号，以调节编码称为III型分泌系统的分子注射器的基因的表达，从而导致感染性结肠炎和炎症。半乳糖醛酸既是营养物，又是指示胃肠道内微生物与病原菌关系的信号。这项工作强调，饮食中糖的可利用性差异会影响微生物群和肠道病原体之间的关系，以及疾病的后果。
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