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首页> 外文期刊>Infection and immunity >Role of Deoxyribose Catabolism in Colonization of the Murine Intestine by Pathogenic Escherichia coli Strains
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Role of Deoxyribose Catabolism in Colonization of the Murine Intestine by Pathogenic Escherichia coli Strains

机译：脱氧核糖代谢在致病性大肠杆菌菌株对小鼠肠道的定殖中的作用

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We previously suggested that the ability to metabolize deoxyribose, a phenotype encoded by the deoK operon, is associated with the pathogenic potential of Escherichia coli strains. Carbohydrate metabolism is thought to provide the nutritional support required for E. coli to colonize the intestine. We therefore investigated the role of deoxyribose catabolism in the colonization of the gut, which acts as a reservoir, by pathogenic E. coli strains. Molecular and biochemical characterization of 1,221 E. coli clones from various collections showed this biochemical trait to be common in the E. coli species (33.6%). However, multivariate analysis evidenced a higher prevalence of sugar-metabolizing E. coli clones in the stools of patients from countries in which intestinal diseases are endemic. Diarrhea processes frequently involve the destruction of intestinal epithelia, so it is plausible that such clones may be positively selected for in intestines containing abundant DNA, and consequently deoxyribose. Statistical analysis also indicated that symptomatic clinical disorders and the presence of virulence factors specific to extraintestinal pathogenic E. coli were significantly associated with an increased risk of biological samples and clones testing positive for deoxyribose. Using the streptomycin-treated-mouse model of intestinal colonization, we demonstrated the involvement of the deoK operon in gut colonization by two pathogenic isolates (one enteroaggregative and one uropathogenic strain). These results, indicating that deoxyribose availability promotes pathogenic E. coli growth during host colonization, suggest that the acquisition of this trait may be an evolutionary step enabling these pathogens to colonize and persist in the mammalian intestine.
机译：我们以前曾提出，代谢 deoK 操纵子的表型脱氧核糖的能力与大肠杆菌菌株的致病潜力有关。碳水化合物代谢被认为可以提供 E所需的营养支持。大肠杆菌在肠道内定植。因此，我们研究了脱氧核糖分解代谢在病原体E引起的肠道菌落定殖中的作用，该菌落作为储库。大肠杆菌菌株。 1,221 E的分子和生化特征。来自不同集合的大肠杆菌克隆显示出这种生化特性在 E中很常见。大肠菌（33.6％）。但是，多变量分析表明糖代谢 E的患病率较高。肠道疾病流行国家/地区患者粪便中的大肠杆菌克隆。腹泻过程通常涉及肠道上皮的破坏，因此可以在含有大量DNA的肠道中选择阳性克隆，从而对其中的脱氧核糖进行阳性选择。统计分析还表明，症状性临床疾病和肠外致病性 E特异的毒力因子的存在。大肠杆菌与生物学样品和脱氧核糖呈阳性的克隆的风险增加显着相关。使用链霉素处理的小鼠肠道菌落模型，我们证明了 deoK 操纵子参与了两种病原菌（一种是肠道聚集菌，另一种是尿毒症菌）在肠道定殖。这些结果表明，脱氧核糖的可用性促进了致病性 E。细菌在宿主定殖过程中的生长表明该特性的获得可能是使这些病原体能够定殖并在哺乳动物肠道中持久的进化步骤。

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