Impact of the rpoS genotype for acid resistance patterns of pathogenic and probiotic Escherichia coli.
Impact of the rpoS genotype for acid resistance patterns of pathogenic and probiotic Escherichia coli.
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DOI：
10.1186/1471-2180-7-21
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发表时间：
2007-03-26
期刊：
影响因子：
4.2
通讯作者：
Gunzer F
中科院分区：
文献类型：
--
作者：
Coldewey SM;Hartmann M;Schmidt DS;Engelking U;Ukena SN;Gunzer F
肠出血性大肠杆菌 (EHEC) 是产生志贺毒素 (Stx) 的大肠杆菌 (STEC) 的一个亚群，可能引起严重肠炎和溶血性尿毒症综合征 (HUS)，并通过受污染的食物经口传播或在人与人之间传播。众所周知，感染剂量非常低，需要大多数细菌才能穿过胃酸屏障。因此，耐酸性是肠出血性大肠杆菌毒力的重要机制。它也应该是用于治疗目的的大肠杆菌菌株的相关特征，例如益生菌大肠杆菌 Nissle 1917 (EcN)。在大肠杆菌和相关肠道细菌中，已广泛证明由 rpoS 基因编码的替代 sigma 因子 σS 充当介导对各种环境应激因素的抵抗力的主调节因子。使用高毒力 EHEC O26:H11 患者分离株的 rpoS 缺失突变体和 O157:H7 血清型的测序原型 EHEC EDL933 (ATCC 700927)，我们研究了功能性 rpoS 基因对在这些菌株中协调对酸应激的令人满意的反应的影响。然后，我们对益生菌 EcN 的 rpoS 和从预先研究耐酸性的 STEC 分离株中选择的 5 个 rpoS 基因进行了功能表征。首先，我们发现 EHEC EDL933 的 ATCC 分离株 700927 在 rpoS 中存在点突变，该点突变不存在于已发表的序列中，导致终止密码子过早出现。此外，令我们惊讶的是，一种 STEC 菌株以及 EcN 在我们的测试环境中对酸敏感，尽管它们克隆的 rpoS 基因可以有效补充 rpoS 缺失突变体的酸敏感性。已测序的 EHEC EDL933 的减毒对于计划使用该原型菌株进行体外或体内研究的任何人来说可能都很重要。此外，我们的数据支持最近发表的观察结果，即单个大肠杆菌分离株能够显着调节其耐酸性表型，而与其 rpoS 基因型无关。
Enterohemorrhagic E. coli (EHEC), a subgroup of Shiga toxin (Stx) producing E. coli (STEC), may cause severe enteritis and hemolytic uremic syndrome (HUS) and is transmitted orally via contaminated foods or from person to person. The infectious dose is known to be very low, which requires most of the bacteria to survive the gastric acid barrier. Acid resistance therefore is an important mechanism of EHEC virulence. It should also be a relevant characteristic of E. coli strains used for therapeutic purposes such as the probiotic E. coli Nissle 1917 (EcN). In E. coli and related enteric bacteria it has been extensively demonstrated, that the alternative sigma factor σS, encoded by the rpoS gene, acts as a master regulator mediating resistance to various environmental stress factors. Using rpoS deletion mutants of a highly virulent EHEC O26:H11 patient isolate and the sequenced prototype EHEC EDL933 (ATCC 700927) of serotype O157:H7 we investigated the impact of a functional rpoS gene for orchestrating a satisfactory response to acid stress in these strains. We then functionally characterized rpoS of probiotic EcN and five rpoS genes selected from STEC isolates pre-investigated for acid resistance. First, we found out that ATCC isolate 700927 of EHEC EDL933 has a point mutation in rpoS, not present in the published sequence, leading to a premature stop codon. Moreover, to our surprise, one STEC strain as well as EcN was acid sensitive in our test environment, although their cloned rpoS genes could effectively complement acid sensitivity of an rpoS deletion mutant. The attenuation of sequenced EHEC EDL933 might be of importance for anyone planning to do either in vitro or in vivo studies with this prototype strain. Furthermore our data supports recently published observations, that individual E. coli isolates are able to significantly modulate their acid resistance phenotype independent of their rpoS genotype.
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影响因子：
3.2
作者：
GAY, P;LECOQ, D;HOCH, JA
通讯作者：
HOCH, JA
影响因子：
24.5
作者：
Kruis, W;Fric, P;Schulze, J
通讯作者：
Schulze, J
影响因子：
3.2
作者：
LANGE, R;FISCHER, D;HENGGEARONIS, R
通讯作者：
HENGGEARONIS, R
影响因子：
9.4
作者：
FRANKE, S;HARMSEN, D;KARCH, H
通讯作者：
KARCH, H
影响因子：
3.1
作者：
Gunzer, F;Bohn, U;Donohue-Rolfe, A
通讯作者：
Donohue-Rolfe, A