The function of Autoinducer-2 (AI-2) which acts as the signal molecule of LuxS-mediated quorum sensing, is regulated through the lsr operon (which includes eight genes: lsrK, lsrR, lsrA, lsrC, lsrD, lsrB, lsrF, and lsrG). However, the functions of the lsr operon remain unclear in avian pathogenic Escherichia coli (APEC), which causes severe respiratory and systemic diseases in poultry. In this study, the presence of the lsr operon in 60 APEC clinical strains (serotypes O1, O2, and O78) was investigated and found to be correlated with serotype and has the highest detection rate in O78. The AI-2 binding capacity of recombinant protein LsrB of APEC (APEC-LsrB) was verified and was found to bind to AI-2 in vitro. In addition, the lsr operon was mutated in an APEC strain (APEC94Δlsr(Cm)) and the mutant was found to be defective in motility and AI-2 uptake. Furthermore, deletion of the lsr operon attenuated the virulence of APEC, with the LD50 of APEC94Δlsr(Cm) decreasing 294-fold compared with wild-type strain APEC94. The bacterial load in the blood, liver, spleen, and kidneys of ducks infected with APEC94Δlsr(Cm) decreased significantly (p < 0.0001). The results of transcriptional analysis showed that 62 genes were up-regulated and 415 genes were down-regulated in APEC94Δlsr(Cm) compared with the wild-type strain and some of the down-regulated genes were associated with the virulence of APEC. In conclusion, our study suggests that lsr operon plays a role in the pathogenesis of APEC.

中文翻译：

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Lsr操纵子与禽病原性大肠杆菌中的AI-2转移和致病性相关。

通过lsr操纵子（包括8个基因：lsrK，lsrR，lsrA，lsrC，lsrD，lsrB，lsrF，和lsrG）。但是，lsr操纵子的功能在禽致病性大肠杆菌（APEC）中仍然不清楚，后者会导致家禽严重的呼吸系统疾病和系统性疾病。在这项研究中，调查了60个APEC临床菌株（血清型O1，O2和O78）中lsr操纵子的存在，发现它们与血清型相关，并且在O78中检出率最高。验证了APEC的重组蛋白LsrB（APEC-LsrB）的AI-2结合能力，并发现其在体外与AI-2结合。此外，将lsr操纵子在APEC菌株（APEC94Δlsr（Cm））中突变，发现该突变体在运动性和AI-2吸收方面存在缺陷。此外，lsr操纵子的缺失减弱了APEC的毒性，与野生型菌株APEC94相比，APEC94Δlsr（Cm）的LD50降低了294倍。感染APEC94Δlsr（Cm）的鸭子的血液，肝脏，脾脏和肾脏中的细菌负荷显着降低（p <0.0001）。转录分析结果表明，与野生型菌株相比，APEC94Δlsr（Cm）中有62个基因被上调，而415个基因被下调，其中一些下调的基因与APEC的毒力有关。总之，我们的研究表明lsr操纵子在APEC的发病机理中起作用。与野生型菌株APEC94相比，APEC94Δlsr（Cm）的LD50降低294倍。感染APEC94Δlsr（Cm）的鸭子的血液，肝脏，脾脏和肾脏中的细菌负荷显着降低（p <0.0001）。转录分析结果表明，与野生型菌株相比，APEC94Δlsr（Cm）中有62个基因被上调，而415个基因被下调，其中一些下调的基因与APEC的毒力有关。总之，我们的研究表明lsr操纵子在APEC的发病机理中起作用。与野生型菌株APEC94相比，APEC94Δlsr（Cm）的LD50降低294倍。感染APEC94Δlsr（Cm）的鸭子的血液，肝脏，脾脏和肾脏中的细菌负荷显着降低（p <0.0001）。转录分析结果表明，与野生型菌株相比，APEC94Δlsr（Cm）中有62个基因被上调，而415个基因被下调，其中一些下调的基因与APEC的毒力有关。总之，我们的研究表明lsr操纵子在APEC的发病机理中起作用。转录分析结果表明，与野生型菌株相比，APEC94Δlsr（Cm）中有62个基因被上调，而415个基因被下调，其中一些下调的基因与APEC的毒力有关。总之，我们的研究表明lsr操纵子在APEC的发病机理中起作用。转录分析结果表明，与野生型菌株相比，APEC94Δlsr（Cm）中有62个基因被上调，而415个基因被下调，其中一些下调的基因与APEC的毒力有关。总之，我们的研究表明lsr操纵子在APEC的发病机理中起作用。