Quorum sensing-1 signaling of N-hexanoyl-l-homoserine lactone contributes to virulence in avian pathogenic Escherichia coli
Quorum sensing-1 signaling of N-hexanoyl-l-homoserine lactone contributes to virulence in avian pathogenic Escherichia coli
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N-己酰基-L-高丝氨酸内酯的群体感应-1信号传导有助于禽致病性大肠杆菌的毒力
DOI：
10.1007/s00203-021-02571-5
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发表时间：
2021-07
影响因子：
2.8
通讯作者：
Zhu Guoqiang
中科院分区：
文献类型：
--
作者：
Yang Yang;Zhang Xin;Zhang Binbin;Zhou Mingxu;Duan Qiangde;Li Zhendong;Zhang Xinyi;Zhu Guoqiang
禽致病性大肠杆菌（APEC）引起的禽大肠杆菌病在世界范围内的家禽业中最为常见。APEC毒力因子导致发病，群体感应（quorum sensing， QS）系统积极参与这些毒力因子的调控。QS中的信号分子被称为自诱导剂（AIs）。在QS-1中，大肠杆菌编码一个单一的LuxR同源物，即SdiA，但不表达LuxI同源物，一种产生AI-1的酰基-高丝氨酸内酯（AHL）合成酶。禽致病性大肠杆菌（APEC）通过调控其毒力基因表达来响应外源AHL，但AHL和QS-1的调控机制尚不清楚。本研究以APEC CE129分离株为对照菌株，将小肠结肠炎耶尔森菌yenI基因表达到APEC CE129中。CE129/pyenI被赋予产生AHL信号的能力。利用λRed重组系统构建了框内缺失AHL受体基因的CE129突变株，该突变株丧失了AHL的感知能力。本研究旨在探讨QS-1对APEC菌株毒力的作用，阐明QS-1/AHL信号对APEC菌株毒力的调控作用。粘附性和侵袭性试验显示，QS-1影响APEC粘附性和生存能力。C6HSL也抑制了APEC生物膜的形成。有趣的是，与产肠毒素大肠杆菌和肠出血性大肠杆菌（分别为ETEC和EHEC）相比，APEC表现出不同的耐酸表型和鞭毛表达。这些发现增强了我们对QS机制的理解。
Avian pathogenic E. coli (APEC) caused avian colibacillosis is mostly common in poultry industry worldwide. APEC virulence factors lead to pathogenesis and the quorum sensing (QS) system is actively involved in the regulation of these virulence factors. Signaling molecules in QS are known as autoinducers (AIs). In QS-1, E. coli encodes a single LuxR homolog, i.e., SdiA, but does not express the LuxI homolog, an acyl-homoserine lactone (AHL) synthase of producing AI-1. Avian pathogenic E. coli (APEC) regulates its virulence genes expression in response to exogenous AHLs, but regulatory mechanisms of AHL and QS-1 are still unknown. This study targeted the APEC CE129 isolate as the reference strain, and the Yersinia enterocolitica yenI gene was expressed into APEC CE129. CE129/pyenI was conferred the ability to produce AHL signal. The CE129 SdiA mutant strain with an in-frame sdiA (AHL receptor) gene deletion was constructed by a λRed recombination system, which lost the ability to sense AHL. The goal of this study was to explore the function of QS-1 upon virulence and elucidate the regulatory effect of QS-1/AHL signals in the APEC strain. Adherence and invasion assays revealed that QS-1 affected APEC adherence and survival ability. APEC biofilm formation was also suppressed under C6HSL. Interestingly, APEC exhibited different phenotypes of acid tolerance and flagella expression when compared to enterotoxigenic E. coli or enterohemorrhagic E. coli (ETEC and EHEC, respectively). These findings enhance our understanding of the QS mechanism.
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影响因子：
7.5
作者：
M. Täuber;M. Sande
通讯作者：
M. Täuber;M. Sande
影响因子：
2.2
作者：
B. Stecher;S. Hapfelmeier;C. Müller;M. Kremer;T. Stallmach;W. Hardt
通讯作者：
B. Stecher;S. Hapfelmeier;C. Müller;M. Kremer;T. Stallmach;W. Hardt
luxS基因在禽致病性大肠杆菌发病机制中的作用
影响因子：
3.8
作者：
Han, Xiangan;Bai, Hao;Yu, Shengqing
通讯作者：
Yu, Shengqing
影响因子：
2.6
作者：
HAVENS, PL;DUNNE, WM;BURD, EM
通讯作者：
BURD, EM
Autoinducer2 影响禽类致病性大肠杆菌中甲氧苄氨嘧啶-磺胺甲恶唑的敏感性，依赖于叶酸合成相关途径。
影响因子：
3.4
作者：
Yu L;Li W;Zhang M;Cui Y;Chen X;Ni J;Yu L;Shang F;Xue T
通讯作者：
Xue T