The luxS gene functions in the pathogenesis of avian pathogenic Escherichia coli

文献类型： 外文期刊

第一作者： Han, Xiangan

作者： Han, Xiangan;Bai, Hao;Liu, Lei;Dong, Hongliang;Liu, Rui;Song, Jun;Ding, Chan;Liu, Haiwen;Yu, Shengqing;Qi, Kezong

作者机构：

关键词： Avian pathogenic Escherichia coli;Quorum sensing;luxS mutant;Pathogenicity

期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.738； 五年影响因子：3.663 ）

ISSN： 0882-4010

年卷期： 2013 年 55 卷

页码：

收录情况： SCI

摘要： Avian pathogenic Escherichia coli (APEC) causes avian colibacillosis, the most significant infectious bacterial disease of poultry worldwide. LuxS, the product of the luxS gene, mediates the quorum sensing (QS) mechanism. This involves the production of autoinducer-2 (AI-2), which regulates important physiological traits and a variety of adaptive processes in different bacteria. In this study, a luxS gene deleted APEC mutant strain, Delta DE17, was constructed using strain DE17. Analysis of bioluminescence indicated that deletion of the luxS gene abolished the production of the QS signal AI-2 in the bacteria. Further studies showed that deletion of the luxS gene in DE17 reduced the bacterial virulence by 31.5-fold in ducklings, based on the measurement of the 50% lethal dose. The mutant strain reduced significantly the abilities of adherence and invasion, by 50.0% and 40.7% respectively, compared with the wild strain DE17. The mutant strain also showed reduced survival in vivo: the bacterial loads of the mutant strain in infected liver, spleen and blood were 46.4-fold, 5.2-fold, and 3.7-fold reduced, respectively, compared with the wild-type strain DE17. Real-time polymerase chain reaction (PCR) demonstrated further that the mRNA levels of the virulence-related genes iucD, fyuA, vat, ompA, iss, fimC and tsh were significantly decreased in the mutant strain Delta DE17, when compared with DE17 (p < 0.05). In addition, the deletion of the luxS gene reduced the motility of the bacterium. This study suggests that the luxS gene functions in the pathogenesis of diseases caused by avian pathogenic E. coli. (C) 2012 Elsevier Ltd. All rights reserved.

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