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Conditioning of Uropathogenic Escherichia coli for Enhanced Colonization of Host

机译：调节致病性大肠埃希氏大肠杆菌的宿主

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While in transit within and between hosts, uropathogenic Escherichia coli (UPEC) encounters multiple stresses, including substantial levels of nitric oxide and reactive nitrogen intermediates. Here we show that UPEC, the primary cause of urinary tract infections, can be conditioned to grow at higher rates in the presence of acidified sodium nitrite (ASN), a model system used to generate nitrosative stress. When inoculated into the bladder of a mouse, ASN-conditioned UPEC bacteria are far more likely to establish an infection than nonconditioned bacteria. Microarray analysis of ASN-conditioned bacteria suggests that several NsrR-regulated genes and other stress- and polyamine-responsive factors may be partially responsible for this effect. Compared to K-12 reference strains, most UPEC isolates have increased resistance to ASN, and this resistance can be substantially enhanced by addition of the polyamine cadaverine. Nitrosative stress, as generated by ASN, can stimulate cadaverine synthesis by UPEC, and growth of UPEC in cadaverine-supplemented broth in the absence of ASN can also promote UPEC colonization of the bladder. These results suggest that UPEC interactions with polyamines or stresses such as reactive nitrogen intermediates can in effect reprogram the bacteria, enabling them to better colonize the host.
机译：泌尿道致病性大肠埃希氏菌（UPEC）在宿主内部和宿主之间运输时会遇到多种压力，包括大量的一氧化氮和活性氮中间体。在这里，我们表明，在酸性亚硝酸钠（ASN）（一种用于产生亚硝化应激的模型系统）的存在下，UPEC（尿路感染的主要原因）可以被调节成以更高的速率生长。当将ASN条件化的UPEC细菌接种到小鼠的膀胱中时，其感染可能性要比非条件化细菌高得多。对ASN条件细菌的微阵列分析表明，几种NsrR调控的基因以及其他应激和多胺反应性因子可能部分负责这种作用。与K-12参考菌株相比，大多数UPEC分离株对ASN的抵抗力增强，并且通过添加多胺尸胺可以大大提高这种抵抗力。由ASN产生的亚硝酸盐胁迫可以刺激UPEC合成尸胺，在缺少ASN的尸胺补充肉汤中UPEC的生长也可以促进UPEC在膀胱中的定植。这些结果表明，UPEC与多胺或应激（例如活性氮中间体）的相互作用可以有效地重编程细菌，从而使其能够更好地定殖于宿主。

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