QseBC regulates in vitro and in vivo virulence of Aeromonas hydrophila in response to norepinephrine
文献类型： 外文期刊
作者： Qin, Ting 1 ; Chen, Kai 1 ; Xi, Bingwen 2 ; Pan, Liangkun 1 ; Xie, Jun 1 ;
作者机构： 1.Chinese Acad Fishery Sci, Freshwater Fisheries Res Ctr, Key Lab Freshwater Fisheries & Germplasm Resource, Minist Agr, Wuxi 214081, Peoples R China
2.Chinese Acad Fishery Sci, Freshwater Fisheries Res Ctr, Key Lab Integrated Rice Fish Farming Ecol, Minist Agr & Rural Affairs, Wuxi 214081, Peoples R China
3.Chinese Acad Fishery Sci, Freshwater Fisheries Res Ctr, Key Lab Aquat Anim Nutr & Hlth, Wuxi 214081, Peoples R China
4.Nanjing Agr Univ, Wuxi Fisheries Coll, Wuxi 214081, Peoples R China
关键词： Aeromonas hydrophila; QseBC; Norepinephrine; Virulence
期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.8； 五年影响因子：4.0 ）
ISSN： 0882-4010
年卷期： 2023 年 174 卷
页码：
收录情况： SCI
摘要： 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 hydro-phila, 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 demon-strated that deletion of qseB and qseC significantly inhibited NE-promoted growth, biofilm formation, and he-molytic activity of A. hydrophila. The adhesion ability of Delta qseB and Delta qseC 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.
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