Quorum sensing controls expression of the type III secretion gene transcription and protein secretion in enterohemorrhagic and enteropathogenic Escherichia coli
Quorum sensing controls expression of the type III secretion gene transcription and protein secretion in enterohemorrhagic and enteropathogenic Escherichia coli
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DOI：
10.1073/pnas.96.26.15196
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发表时间：
1999-12-21
影响因子：
11.1
通讯作者：
Kaper, JB
中科院分区：
文献类型：
--
作者：
Sperandio, V;Mellies, JL;Kaper, JB
肠出血性大肠杆菌O157：H7和肠致病性大肠杆菌。大肠杆菌在肠细胞中引起一种特征性的组织病理学，称为附着和消失。附着和消退病变由肠上皮细胞消退基因座（LEE）致病岛编码，其编码III型分泌系统、内膜蛋白肠定殖因子和从细菌易位到宿主上皮细胞的易位的内膜蛋白受体蛋白。使用lacZ报告基因融合，我们表明，表达的LEE操纵子编码的III型分泌系统，易位的内膜受体，和内膜是由群体感应在两个肠出血性大肠杆菌：大肠杆菌和肠致病性E. luxS基因最近被证明负责在哈氏弧菌和大肠杆菌群体感应系统中产生自诱导物，其负责LEE操纵子的调节，如luxS基因的突变和互补所示。群体感应对肠道定植因子的调节可能在这些微生物引起的疾病的发病机制中起重要作用。这些结果表明，肠道定植的E。coliO157：H7，其感染剂量非常低，可以通过非致病性E.大肠杆菌的正常肠道植物群。
Enterohemorrhagic Escherichia coli O157:H7 and enteropathogenic E. coli cause a characteristic histopathology in intestinal cells known as attaching and effacing. The attaching and effacing lesion is encoded by the Locus of Enterocyte Effacement (LEE) pathogenicity island, which encodes a type III secretion system, the intimin intestinal colonization factor, and the translocated intimin receptor protein that is translocated from the bacterium to the host epithelial cells. Using lacZ reporter gene fusions, we show that expression of the LEE operons encoding the type III secretion system, translocated intimin receptor, and intimin is regulated by quorum sensing in both enterohemorrhagic: E. coli and enteropathogenic E. coli, The luxS gene recently shown to be responsible for production of autoinducer in the Vibrio harveyi and E, coli quorum-sensing systems is responsible for regulation of the LEE operons, as shown by the mutation and complementation of the luxS gene. Regulation of intestinal colonization factors by quorum sensing could play an important role in the pathogenesis of disease caused by these organisms. These results suggest that intestinal colonization by E. coli O157:H7, which has an unusually low infectious dose, could be induced by quorum sensing of signals produced by nonpathogenic E. coli of the normal intestinal flora.