Key Lab Freshwater Fisheries and Germplasm Resource Utilization, Ministry Agriculture, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China; Key Laboratory of Integrated Rice-Fish Farming Ecology, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China; Key Laboratory of Aquatic Animal Nutrition and Health, Freshwater Fisheries Research Center, Chinese Academy of Fishery Science, Wuxi, 214081, China.
Key Laboratory of Integrated Rice-Fish Farming Ecology, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China; Wuxi Fisheries College, Nanjing Agricultural University, Wuxi, 214081, China.
Microb Pathog. 2023 Jan;174:105914. doi: 10.1016/j.micpath.2022.105914. Epub 2022 Nov 28.
The inter-kingdom communication between host and pathogenic bacteria mediated by the host hormones epinephrine (Epi)/norepinephrine (NE)/autoinducer-3 (AI-3) and transduced by the bacterial two-component signal transduction system QseBC has been well demonstrated in mammalian pathogens. Aeromonas hydrophila, a common opportunistic pathogen in freshwater aquaculture, responds to NE by increased bacterial growth and enhanced virulence. However, the underlying mechanisms remain poorly understood. Our study demonstrated that deletion of qseB and qseC significantly inhibited NE-promoted growth, biofilm formation, and hemolytic activity of A. hydrophila. The adhesion ability of ΔqseB and ΔqseC to J774a.1 cells was significantly decreased compared with the wild-type strain in the presence and absence of NE, whereas NE still enhanced the adhesion ability of the mutant and wild-type strains with a similar effect, suggesting that NE-enhanced cell adhesion was independent of QseBC. Moreover, QseBC did not affect the swimming and swarming motility of A. hydrophila with or without NE. Quantitative real-time PCR analyses revealed the down-regulated expression of some virulence-related genes (hly, ast, act, aerA) in each mutant compared with the wild-type strain in the presence of NE. Tilapia infection experiments indicated that deletion of qseB or qseC weakened NE-promoted virulence of A. hydrophila. In conclusion, our study suggests that NE stimulates the growth, biofilm formation, and hemolytic activity of A. hydrophila and enhances the virulence of the pathogen in fish via the QseBC system.
宿主激素肾上腺素（Epi）/去甲肾上腺素（NE）/自诱导物-3（AI-3）介导的宿主与病原菌之间的跨界通讯，并通过细菌双组分信号转导系统 QseBC 进行转导，在哺乳动物病原体中得到了很好的证明。嗜水气单胞菌是淡水水产养殖中的一种常见机会性病原体，对 NE 的反应是增加细菌生长和增强毒力。然而，其潜在机制仍知之甚少。我们的研究表明，qseB 和 qseC 的缺失显著抑制了 NE 促进的嗜水气单胞菌生长、生物膜形成和溶血活性。与野生型菌株相比，ΔqseB 和 ΔqseC 在存在和不存在 NE 的情况下，对 J774a.1 细胞的粘附能力显著降低，而 NE 仍增强了突变体和野生型菌株的粘附能力，效果相似，表明 NE 增强的细胞粘附与 QseBC 无关。此外，QseBC 不影响有或没有 NE 时嗜水气单胞菌的游泳和群集运动。定量实时 PCR 分析显示，与野生型菌株相比，在存在 NE 的情况下，每个突变体中一些与毒力相关的基因（hly、ast、act、aerA）的表达均下调。罗非鱼感染实验表明，qseB 或 qseC 的缺失削弱了 NE 促进嗜水气单胞菌的毒力。总之，我们的研究表明，NE 通过 QseBC 系统刺激嗜水气单胞菌的生长、生物膜形成和溶血活性，并增强病原体在鱼类中的毒力。
