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首页> 外文期刊>Journal of bacteriology >Genomic Islands of Uropathogenic Escherichia coli Contribute to Virulence
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Genomic Islands of Uropathogenic Escherichia coli Contribute to Virulence

机译：致病性大肠杆菌的基因组岛有助于致病性

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Uropathogenic Escherichia coli (UPEC) strain CFT073 contains 13 large genomic islands ranging in size from 32 kb to 123 kb. Eleven of these genomic islands were individually deleted from the genome, and nine isogenic mutants were tested for their ability to colonize the CBA/J mouse model of ascending urinary tract infection. Three genomic island mutants (ΔPAI-aspV, ΔPAI-metV, and ΔPAI-asnT) were significantly outcompeted by wild-type CFT073 in the bladders and/or kidneys following transurethral cochallenge (P ≤ 0.0139). The PAI-metV mutant also showed significant attenuation in the ability to independently colonize the kidneys (P = 0.0011). Specific genes within these islands contributed to the observed phenotype, including a previously uncharacterized iron acquisition cluster, fbpABCD (c0294 to c0297 [c0294-97]), autotransporter, picU (c0350), and RTX family exoprotein, tosA (c0363) in the PAI-aspV island. The double deletion mutant with deletions in both copies of the fbp iron acquisition operon (Δc0294-97 Δc2518-15) was significantly outcompeted by wild-type CFT073 in cochallenge. Strains with mutations in a type VI secretion system within the PAI-metV island did not show attenuation. The attenuation of the PAI-metV island was localized to genes c3405-10, encoding a putative phosphotransferase transport system, which is common to UPEC and avian pathogenic E. coli strains but absent from E. coli K-12. We have shown that, in addition to encoding virulence genes, genomic islands contribute to the overall fitness of UPEC strain CFT073 in vivo.
机译：致病性大肠埃希氏菌（UPEC）菌株CFT073包含13个大的基因岛，大小从32 kb到123 kb不等。这些基因组岛中的11个分别从基因组中删除，并且测试了9个同基因突变体定殖在升尿路感染的CBA / J小鼠模型中的能力。膀胱中的野生型CFT073明显优于三个基因组岛突变体（ΔPAI- aspV ，ΔPAI- metV 和ΔPAI- asnT ）和/或经尿道胆囊攻击后肾脏（ P ≤0.0139）。 PAI- metV 突变体在独立定居肾脏的能力上也显示出明显的减弱（ P = 0.0011）。这些岛中的特定基因促成观察到的表型，包括先前未表征的铁捕获簇 fbpABCD （c0294至c0297 [c0294-97]），自转运蛋白 picU （c0350 ）和PAI- aspV 岛中的RTX家族外蛋白 tosA （c0363）。在挑战中，野生型CFT073明显胜过在 fbp 铁获取操纵子的两个拷贝中都缺失的双缺失突变体（Δc0294-97Δc2518-15）。在PAI- metV 岛内的VI型分泌系统中突变的菌株未显示出减毒作用。 PAI- metV 岛的衰减定位于基因c3405-10，编码一个假定的磷酸转移酶转运系统，这是UPEC和禽致病性 E 的共同特征。 大肠杆菌菌株，但 E 中没有。 大肠杆菌 K-12。我们已经表明，除了编码毒力基因外，基因组岛还有助于体内UPEC菌株CFT073的整体适应性。

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