文献类型：期刊文献

英文题名：QseBC controls flagellar motility, fimbrial hemagglutination and intracellular virulence in fish pathogen Edwardsiella tarda

作者：Wang, Xin[1];Wang, Qiyao[1];Yang, Minjun[1];Xiao, Jingfan[1];Liu, Qin[1];Wu, Haizhen[1];Zhang, Yuanxing[1]

机构：[1]E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China

年份：2011

卷号：30

期号：3

起止页码：944

外文期刊名：FISH & SHELLFISH IMMUNOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000288888500025)】；

基金：This work was supported by grants from the National High Technology Research and Development Program of China (2008AA092501), Ministry of Agriculture of China (Nos. nyhyzx07 and nycytx-50), the National Special Fund for State Key Laboratory of Bioreactor Engineering (No. 2060204) as well as Shanghai Leading Academic Discipline Project (No. B505).

语种：英文

外文关键词：Edwardsiella tarda; QesBC; Motililty; Hemagglutination; Virulence

摘要：The inter-kingdom communication with the mammalian hosts mediated by autoinducer-3 (AI-3)/epinephrine (Epi)/norepinephrine (NE), and transduced by two-component systems QseBC has recently been described. As a fish pathogen and opportunistic pathogen for human beings. Edwardsiella tarda develops surface structures such as flagellar and fimbriae to cause different hemagglutination phenotypes and serotypes and initiate pathogen-host recognition and invasion process. E. tarda survives within macrophages in fish using type III secretion system (TTSS). Here, the genes of E. tarda two-component system, qseB and qseC, were found to be co-transcribed. Phylogenetic analysis indicated that evolution of QseC strongly correlated to different host niches. Compared with the wild type and their complemented strains, Delta qseB and Delta qseC mutants exhibited significant impaired flagellar motilities. Mammalian Epi was able to stimuli the flagellar motility in E. tarda via QseBC. Hemagglutination caused by fimbriae was induced in Delta qseB but repressed in Delta aseC. Disruption of qseB or qseC down-regulated the intracellular expressions of TTSS elements EseB and EsaC, and impaired their intracellular survival capabilities as well as in vivo competitive abilities. Furthermore, in vitro tests indicated that expression of EseB was induced by Epi via QseBC. Our results revealed that the QseBC system modified the virulence-related surface structures (flagellum, fimbriae and secretion system) and that hormone might stimulate the virulence of the pathogen in fish. (C) 2011 Elsevier Ltd. All rights reserved.