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Unique beta-glucuronidase locus in gut microbiomes of crohn's disease patients and unaffected first-degree relatives

机译：克罗恩病患者和未患一级亲属的肠道菌群中独特的β-葡萄糖醛酸苷酶基因座

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Crohn's disease, an incurable chronic inflammatory bowel disease, has been attributed to both genetic predisposition and environmental factors. A dysbiosis of the gut microbiota, observed in numerous patients but also in at least one hundred unaffected first-degree relatives, was proposed to have a causal role. Gut microbiota beta-D-glucuronidases (EC 3.2.1.33) hydrolyse beta-D-glucuronate from glucuronidated compounds. They include a GUS group, that is homologous to the Escherichia coli GusA, and a BG group, that is homologous to metagenomically identified H11G11 BG and has unidentified natural substrates. H11G11 BG is part of the functional core of the human gut microbiota whereas GusA, known to regenerate various toxic products, is variably found in human subjects. We investigated potential risk markers for Crohn's disease using DNA-sequence-based exploration of the beta-D-glucuronidase loci (GUS or Firmicute H11G11-BG and the respective co-encoded glucuronide transporters). Crohn's disease-related microbiomes revealed a higher frequency of a C7D2 glucuronide transporter (12/13) compared to unrelated healthy subjects (8/32). This transporter was in synteny with the potential harmful GUS beta-D-glucuronidase as only observed in a Eubacterium eligens plasmid. A conserved NH2-terminal sequence in the transporter (FGDFGND motif) was found in 83% of the disease-related subjects and only in 12% of controls. We propose a microbiota-pathology hypothesis in which the presence of this unique beta-glucuronidase locus may contribute to an increase risk for Crohn's disease.
机译：克罗恩氏病是一种无法治愈的慢性炎症性肠病，已被归因于遗传易感性和环境因素。肠道菌群失调在许多患者中也观察到，至少在一百个未受影响的一级亲属中也被认为具有因果关系。肠道菌群β-D-葡萄糖醛酸酶（EC 3.2.1.33）从葡萄糖醛酸化的化合物水解β-D-葡萄糖醛酸。它们包括与大肠杆菌GusA同源的GUS组和与宏基因组学鉴定的H11G11 BG同源且具有未鉴定的天然底物的BG组。 H11G11 BG是人类肠道菌群功能核心的一部分，而已知可再生各种有毒产物的GusA在人类受试者中的含量却有所不同。我们使用基于DNA序列的β-D-葡糖醛酸糖苷酶基因座（GUS或Firmicute H11G11-BG以及各自的共编码葡糖醛酸苷转运蛋白）研究了克罗恩病的潜在危险标记。与不相关的健康受试者（8/32）相比，克罗恩病相关的微生物群显示C7D2葡糖醛酸苷转运蛋白的频率更高（12/13）。该转运蛋白与潜在有害的GUSβ-D-葡糖醛酸糖苷酶协同作用，仅在Eubacterium eligens质粒中观察到。在83％的疾病相关受试者中和仅在12％的对照中发现了转运蛋白（FGDFGND基序）中保守的NH2末端序列。我们提出了一种微生物群落病理学假说，其中这种独特的β-葡萄糖醛酸苷酶基因座的存在可能会增加克罗恩氏病的风险。

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    Anba Mondoloni, Jamila;

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  • 年度 2016
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