Xu Ziheng, Wang Can, Wang Min, Liang Jingzhen, Li Changcheng, Chen Wenyan, Wei Ping
Institute for Poultry Science and Health, Guangxi University, Nanning 530004, China; School of Public Health and Management, Guangxi Key Laboratory of Translational Medicine for Treating High-incidence Infectious Diseases with Integrative Medicine, Guangxi Key Laboratory of Marine Drugs, Guangxi University of Chinese Medicine, Nanning 530200, China.
Institute for Poultry Science and Health, Guangxi University, Nanning 530004, China.
Poult Sci. 2025 Apr;104(4):104972. doi: 10.1016/j.psj.2025.104972. Epub 2025 Mar 7.
Understanding the antimicrobial resistance (AMR) mechanism of Salmonella pullorum (SP), which is widespread among yellow chickens in China, is crucial for reducing significant economic losses in the industry. In this study, we explored the AMR mechanism by which the LuxS/AI-2-mediated quorum sensing (QS) system regulates the AcrAB-TolC efflux pump in the SP. The results showed that the luxS gene and the signaling molecule AI-2 had no effect on the growth of the SP strains. However, the luxS gene knockout strain (SP129∆luxS) was sensitive to antimicrobials (ampicillin, methoxypyrimidine, sulfaisoxazole, trimethoprim/sulfamethoxazole and nalidixic acid), whereas SP129 was resistant. The SP129 strain was resistant to antimicrobials which had previously been proved to be sensitive to the antimicrobials following incubation with AI-2. Moreover, the expression levels of the soxS, acrA, and acrB genes, as well as the SoxS protein were significantly increased by knocking out the luxS gene or by incubating with Al-2. Crucially, there was no interaction between the LuxS protein and the SoxS or SoxR proteins. However, these two proteins were found to be bound to AI-2 via hydrogen bonds. In summary, AMR in SP isolates was enhanced by AI-2 through the promotion of the the expression of the soxS gene and the SoxS protein, activating the efflux pump. Exploring the AMR mechanism of the SP strain provides important baseline information for controlling outbreaks of yellow chicken salmonellosis.
了解在中国黄羽鸡中广泛存在的鸡白痢沙门氏菌（SP）的抗菌耐药性（AMR）机制，对于减少该行业的重大经济损失至关重要。在本研究中，我们探索了LuxS/AI-2介导的群体感应（QS）系统调节SP中AcrAB-TolC外排泵的AMR机制。结果表明，luxS基因和信号分子AI-2对SP菌株的生长没有影响。然而，luxS基因敲除菌株（SP129∆luxS）对抗菌药物（氨苄青霉素、甲氧嘧啶、磺胺异恶唑、甲氧苄啶/磺胺甲恶唑和萘啶酸）敏感，而SP129具有抗性。SP129菌株对先前已被证明敏感的抗菌药物产生抗性，在与AI-2孵育后则对这些抗菌药物敏感。此外，通过敲除luxS基因或与Al-2孵育，soxS、acrA和acrB基因以及SoxS蛋白的表达水平显著增加。至关重要的是，LuxS蛋白与SoxS或SoxR蛋白之间没有相互作用。然而，发现这两种蛋白通过氢键与AI-2结合。总之，AI-2通过促进soxS基因和SoxS蛋白的表达来增强SP分离株中的AMR，从而激活外排泵。探索SP菌株的AMR机制为控制黄羽鸡沙门氏菌病的爆发提供了重要的基线信息。
