作 者：
孟雨潇;秦婷;习丙文;陈凯;谢骏;潘良坤
关键词：
嗜水气单胞菌;QseBC双组分调控系统;去甲肾上腺素;ΔqseC;毒力因子
摘 要：
QseBC是一种普遍存在于细菌的双组分调控系统(two-component regulatory system,TCS),能感应细胞外环境因子信号,在调控细菌毒力中发挥着重要作用。为了研究嗜水气单胞菌(Aeromonas hydrophila)QseC在识别和响应宿主应激激素去甲肾上腺素(norepinephrine,NE)及其对毒力因子表达的调控作用,本实验首先构建了嗜水气单胞菌NJ-35缺失突变株ΔqseC与互补株qseC+,分析了在NE诱导下野生株和突变株的体外毒力因子表达和鱼体死亡率的变化。结果表明,qseC的缺失抑制了NE对嗜水气单胞菌的促生长作用,降低了NE对生物膜形成能力和溶血活性的增强作用及其对罗非鱼的致死率,而对运动性、脂肪酶与蛋白酶活性没有产生显著影响。本实验明确了嗜水气单胞菌QseC能够响应NE,从而调节菌株的毒力,对全面认识嗜水气单胞菌的致病机理及其与宿主的互作机制有着重要意义,并为探索疾病防控新技术奠定相关理论基础。
译 名：
Role of sensor histidine kinase QseC of Aeromonas hydrophila in response to norepinephrine
作 者：
MENG Yuxiao;QIN Ting;XI Bingwen;CHEN Kai;XIE Jun;PAN Liangkun;Wuxi Fisheries College,Nanjing Agricultural University;Freshwater Fisheries Research Center,Chinese Academy of Fishery Sciences;Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization,Ministry of Agriculture and Rural Affairs;
关键词：
Aeromonas hydrophila;;QseBC two-component regulatory system;;norepinephrine;;ΔqseC;;virulence
摘 要：
To date, microbial endocrinology has revealed that many microorganisms have evolved specific mechanisms to sense and respond to stress hormones. Catecholamine stress hormones have been demonstrated to stimulate bacterial growth and virulence-related gene expression. In bacteria, the QseBC two-component system is widely used in signal transduction mechanisms, which have an important impact on bacterial virulence. In this signaling system, the sensor histidine kinase QseC is a bacterial receptor for the host epinephrine(Epi)/norepinephrine(NE), which activates virulence genes in response to interkingdom cross-signaling. In Aeromonas hydrophila NJ-35, NE exhibited the strongest growth stimulation and enhanced virulence. However, it remains poorly understood whether the QseBC two-component system is involved in the recognition and response process of A. hydrophila NJ-35 to NE. To determine whether QseC recognizes NE and regulates bacterial virulence, in this study, we constructed a qseC gene deletion mutant of A. hydrophila NJ-35(ΔqseC) and a complement strain(qseC+), which were tested in both in vitro and in vivo toxicity under NE induction. Our data provide evidence that the growth-promoting effect of NE on ΔqseC was significantly higher than that of the wild-type strain NJ-35, and the biofilm formation ability of ΔqseC was remarkably decreased compared to that of the wild-type strain and complement strain qseC+(P<0.01), with or without NE. Notably, ΔqseC was completely deficient in the promotion of the biofilm formation activity by NE, revealing that QseC was necessary for NE to regulate the biofilm formation of A. hydrophila NJ-35. Additionally, the hemolytic activity of ΔqseC was strikingly increased(P<0.01), but still lower than that of the wild strain NJ-35 and complement strain qseC+ caused by NE, showing that except for QseC,NE could regulate the hemolytic activity of A. hydrophila NJ-35 through another non-QseC pathway. Furthermore,NE can dramatically increase the mortality of the wild-type strain NJ-35 against tilapia, while the deletion of the qseC gene inhibited the enhanced-virulence by NE. However, there were no significant differences in the motility,lipase activity, or protease activity between the wild type strain and mutant △qseC. In conclusion, the deletion of the qseC gene inhibited the NE-stimulated growth and virulence of A. hydrophila NJ-35, indicating that QseC could regulate the pathogenicity of A. hydrophila by recognizing and responding to NE. It is crucial for our study to comprehensively understand the pathogenesis of A. hydrophila and the mechanisms behind the interactions between pathogens and their hosts. This study provides the theoretical foundations for new technologies for prevention and control strategies against bacterial diseases.
