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.

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 (QS) 系统积极参与这些毒力因子的调节。QS 中的信号分子被称为自诱导剂 (AI)。在 QS-1 中，大肠杆菌编码单个 LuxR 同源物，即 SdiA，但不表达 LuxI 同源物，即产生 AI-1 的酰基高丝氨酸内酯 (AHL) 合酶。禽致病性大肠杆菌(APEC) 响应外源性 AHL 调节其毒力基因表达，但 AHL 和 QS-1 的调节机制尚不清楚。本研究以 APEC CE129 分离株为参考菌株，Yersinia enterocolitica YenI基因在 APEC CE129 中表达。CE129/p yenI被赋予产生AHL信号的能力。具有框内sdiA（AHL受体）基因缺失的CE129 SdiA突变株是通过λRed重组系统构建的，该系统失去了感知AHL的能力。本研究的目的是探索 QS-1 对毒力的作用并阐明 QS-1/AHL 信号在 APEC 菌株中的调节作用。依从性和侵袭性分析表明，QS-1 影响 APEC 的依从性和生存能力。在 C6HSL 下，APEC 生物膜的形成也受到抑制。有趣的是，与产肠毒素大肠杆菌或肠出血性大肠杆菌相比，APEC 表现出不同的耐酸表型和鞭毛表达（分别为 ETEC 和 EHEC）。这些发现增强了我们对 QS 机制的理解。