Escherichia coli O157:H7 Lacking the qseBC-Encoded Quorum-Sensing System Outcompetes the Parental Strain in Colonization of Cattle Intestines
Escherichia coli O157:H7 Lacking the qseBC-Encoded Quorum-Sensing System Outcompetes the Parental Strain in Colonization of Cattle Intestines
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DOI：
10.1128/aem.03198-13
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发表时间：
2014-03-01
影响因子：
4.4
通讯作者：
Casey, T. A.
中科院分区：
文献类型：
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作者：
Sharma, V. K.;Casey, T. A.
qseBC 编码的群体感应系统可调节大肠杆菌 O157:H7 的运动性，以响应细菌自诱导剂 3 (AI-3) 和哺乳动物应激激素肾上腺素 (E) 和去甲肾上腺素 (NE)。 qseC 基因编码一种感觉激酶，该激酶响应 AI-3、E 或 NE 进行自磷酸化，随后磷酸化其同源反应调节因子 QseB。在缺乏 QseC 的情况下，QseB 会下调动物模型中的细菌活力和毒力。在这项研究中，我们发现，口服接种大肠杆菌 O157:H7 及其同基因 qseBC 突变体混合物的 8 至 10 个月大的小牛，显示出 qseBC 突变体的粪便排出量显着更高。体外分析显示，在存在或不存在 NE 的情况下，qseBC 突变体和亲本菌株具有相似的生长曲线和运动性。 qseBC 突变体和亲本菌株对 NE 的反应程度以及鞭毛基因 flhD 和 fliC 的表达也相似。与亲本菌株相比，qseBC 突变体中 ler（肠细胞消失位点 [LEE] 的正调节因子）、ler 调节的 espA 基因和 csgA 基因（编码卷曲菌毛）的表达增加。另一方面，在补充有 qseBC 基因的质粒克隆拷贝的 qseBC 突变体中，flhD、fliC、ler、espA 和 csgA 的生长、运动和转录显着降低。因此，体外运动和基因表达数据表明，接近亲代的运动水平、对 NE 的反应能力以及 LEE 和 curli 基因表达的增强可能部分是 qseBC 突变体在小牛中定植和粪便脱落增加的部分原因。
The qseBC-encoded quorum-sensing system regulates the motility of Escherichia coli O157:H7 in response to bacterial autoinducer 3 (AI-3) and the mammalian stress hormones epinephrine (E) and norepinephrine (NE). The qseC gene encodes a sensory kinase that autophosphorylates in response to AI-3, E, or NE and subsequently phosphorylates its cognate response regulator QseB. In the absence of QseC, QseB downregulates bacterial motility and virulence in animal models. In this study, we found that 8- to 10-month-old calves orally inoculated with a mixture of E. coli O157:H7 and its isogenic qseBC mutant showed significantly higher fecal shedding of the qseBC mutant. In vitro analysis revealed similar growth profiles and motilities of the qseBC mutant and the parental strain in the presence or absence of NE. The magnitudes of the response to NE and expression of flagellar genes flhD and fliC were also similar for the qseBC mutant and the parental strain. The expression of ler (a positive regulator of the locus of enterocyte effacement [LEE]), the ler-regulated espA gene, and the csgA gene (encoding curli fimbriae) was increased in the qseBC mutant compared to the parental strain. On the other hand, growth, motility, and transcription of flhD, fliC, ler, espA, and csgA were significantly reduced in the qseBC mutant complemented with a plasmid-cloned copy of the qseBC genes. Thus, in vitro motility and gene expression data indicate that the near-parental level of motility, ability to respond to NE, and enhanced expression of LEE and curli genes might in part be responsible for increased colonization and fecal shedding of the qseBC mutant in calves.