Nitric oxide-enhanced Shiga toxin production was regulated by Fur and RecA in enterohemorrhagic Escherichia coli O157.
Nitric oxide-enhanced Shiga toxin production was regulated by Fur and RecA in enterohemorrhagic Escherichia coli O157.
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DOI：
10.1002/mbo3.461
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发表时间：
2017-08
期刊：
影响因子：
3.4
通讯作者：
Noda M
中科院分区：
文献类型：
--
作者：
Ichimura K;Shimizu T;Matsumoto A;Hirai S;Yokoyama E;Takeuchi H;Yahiro K;Noda M
肠出血性大肠杆菌（EHEC）产生志贺毒素1 （Stx1）和志贺毒素2 （Stx2）。一氧化氮（NO）作为一种抗菌防御分子，在厌氧条件下可促进肠出血性大肠杆菌Stx1和Stx2的产生。虽然EHEC O157具有完整的norV和缺失的norV两种类型的厌氧NO还原酶基因，但在缺失的norV型EHEC中，高浓度的NO （12 - 29 μmol/L，最大稳态浓度）可以增强Stx1的产生，而低浓度的NO （~12 μmol/L，最大稳态浓度）足以在厌氧条件下增强Stx2的产生。这些结果表明，不同浓度阈值的NO诱导了一组离散的Stx1和Stx2生成途径。此外，在完整的norV型肠出血性大肠杆菌中，志贺毒素产生的增强需要更高浓度的NO处理，而在删除的norV型肠出血性大肠杆菌中，志贺毒素产生的增强需要更高浓度的NO处理，这表明特异性norV型在响应NO时志贺毒素产生的增强水平中起着重要作用。最后，在肠出血性大肠杆菌中，Fur的抑制和RecA的激活分别参与了NO增强的Stx1和Stx2的产生。
Enterohemorrhagic Escherichia coli (EHEC) produces Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2). Nitric oxide (NO), which acts as an antimicrobial defense molecule, was found to enhance the production of Stx1 and Stx2 in EHEC under anaerobic conditions. Although EHEC O157 has two types of anaerobic NO reductase genes, an intact norV and a deleted norV, in the deleted norV‐type EHEC, a high concentration of NO (12–29 μmol/L, maximum steady‐state concentration) is required for enhanced Stx1 production and a low concentration of NO (~12 μmol/L, maximum steady‐state concentration) is sufficient for enhanced Stx2 production under anaerobic conditions. These results suggested that different concentration thresholds of NO elicit a discrete set of Stx1 and Stx2 production pathways. Moreover, the enhancement of Shiga toxin production in the intact norV‐type EHEC required treatment with a higher concentration of NO than was required for enhancement of Shiga toxin production in the deleted norV‐type EHEC, suggesting that the specific NorV type plays an important role in the level of enhancement of Shiga toxin production in response to NO. Finally, Fur derepression and RecA activation in EHEC were shown to participate in the NO‐enhanced Stx1 and Stx2 production, respectively.
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