Quorum sensing-1 signaling of N-hexanoyl-l-homoserine lactone contributes to virulence in avian pathogenic Escherichia coli
文献类型： 外文期刊
作者： Yang, Yang 1 ; Zhang, Xin 1 ; Zhang, Binbin 1 ; Zhou, Mingxu 3 ; Duan, Qiangde 1 ; Li, Zhendong 1 ; Zhang, Xinyi 1 ; Zhu, 1 ;
作者机构： 1.Jiangsu Coinnovat Ctr Important Anim Infect Dis &, Yangzhou 225009, Jiangsu, Peoples R China
2.Yangzhou Univ, Coll Vet Med, 12 East Wenhui Rd, Yangzhou 225009, Jiangsu, Peoples R China
3.Jiangsu Acad Agr Sci, Natl Res Ctr Engn & Technol Vet Biol, Inst Vet Immunol & Engn, Nanjing 210014, Peoples R China
4.Minist Sci & Technol, Jiangsu Key Lab Food Qual, Nanjing 210014, Peoples R China
5.Minist Sci & Technol, Safety State Key Lab Cultivat Base, Nanjing 210014, Peoples R China
关键词： APEC; AHL; Quorum sensing; Virulence
期刊名称：ARCHIVES OF MICROBIOLOGY （ 影响因子：2.552； 五年影响因子：2.475 ）
ISSN： 0302-8933
年卷期： 2021 年 203 卷 10 期
页码：
收录情况： SCI
摘要： 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 lambda Red 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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