Conditioning of Uropathogenic Escherichia coli for Enhanced Colonization of Host
Conditioning of Uropathogenic Escherichia coli for Enhanced Colonization of Host
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DOI：
10.1128/iai.01200-08
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发表时间：
2009-05-01
影响因子：
3.1
通讯作者：
Mulvey, Matthew A.
中科院分区：
文献类型：
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作者：
Bower, Jean M.;Gordon-Raagas, Hannah B.;Mulvey, Matthew A.
当在宿主内和宿主之间转运时，尿路致病性大肠杆菌（UPEC）会遇到多种应激，包括大量的一氧化氮和活性氮中间体。在这里，我们表明，UPEC，尿路感染的主要原因，可以调节生长在更高的速度在酸化亚硝酸钠（NO2），用于产生亚硝化应激的模型系统的存在下。当接种到小鼠的膀胱中时，ASN条件化的UPEC细菌比非条件化的细菌更有可能建立感染。ASN条件细菌的微阵列分析表明，几个NSRR调节基因和其他压力和多胺反应因子可能是部分负责这种效果。与K-12参比菌株相比，大多数UPEC分离株具有增加的耐药，并且这种耐药可以通过添加多胺尸胺而显著增强。亚硝化应激，如由Nitrobenzene产生的，可以刺激UPEC合成尸胺，并且在不存在Nitrobenzene的情况下，UPEC在补充尸胺的肉汤中的生长也可以促进UPEC在膀胱中的定殖。这些结果表明，UPEC与多胺或应激（如活性氮中间体）的相互作用可以有效地重新编程细菌，使它们能够更好地定殖宿主。
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.