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Edwardsiella piscicida HigB: A type II toxin that is essential to oxidative resistance, biofilm formation, serum survival, intracellular propagation, and host infection

文献类型： 外文期刊

作者： Xie, Jinhong 1 ; Zhao, Qianyun 2 ; Huang, Huiqin 2 ; Fang, Zaiguang 1 ; Hu, Yonghua 2 ;

作者机构： 1.Hainan Univ, Coll Marine Sci, Key Lab Trop Biol Resources, Minist Educ, Haikou 570228, Hainan, Peoples R China

2.CATAS, Hainan Acad Trop Agr Resource, Inst Trop Biosci & Biotechnol, Haikou 571101, Hainan, Peoples R China

3.Pilot Natl Lab Marine Sci & Technol Qingdao, Lab Marine Biol & Biotechnol, Qingdao, Peoples R China

4.Hainan Prov Key Lab Funct Components Res & Utiliz, Haikou 571101, Hainan, Peoples R China

关键词： Edwardsiella piscicida; Toxin-antitoxin; HigBA; Adversity; Virulence

期刊名称：AQUACULTURE （ 影响因子：3.224； 五年影响因子：3.591 ）

ISSN： 0044-8486

年卷期： 2021 年 535 卷

页码：

收录情况： SCI

摘要： Edwardsiella piscicida (formerly included in E. tarda) is the leading pathogen threatening worldwide fresh and seawater aquaculture industries and has been considered as a model organism for studying intracellular and systemic infections. Toxin-antitoxin (TA) systems are omnipresent in bacteria and participate widely in stress responses, biofilm formation and pathogenicity. However, the roles of TA systems are completely unknown in aquatic pathogenic bacteria. In this study, we identified and characterized a type II TA system HigBA in E. piscicida, where HigB is the toxin and HigA is the antitoxin. higB and higA are expressed in a bicistronic operon. To examine the biological role of HigBA, two markerless higB and higBA in-frame mutant strains, TX01 Delta higB and TX01 Delta higBA, were constructed. Compared to the wild strain TX01, TX01 Delta higB exhibited markedly reduced resistance against oxidative stress, but TX01 Delta higBA remained unchanged; the biofilm growth of TX01 Delta higB was decreased, but that of TX01 Delta higBA was increased. The deletion of higB enhanced bacterial motility but impaired bacterial resistance against host serum killing. In vitro infection experiment showed that the inactivation of higB dramatically abated bacterial capability of adhesion, invasion, and propagation in host cells. Consistently, in vivo experiment suggested that the higB mutation had an obvious negative effect on bacteria dissemination of fish tissues and general virulence. Introduction of a trans-expressed higB restored the lost virulence of TX01 Delta higB. However, the virulence of TX01 Delta higBA was compared to that of TX01. These findings indicate that HigB is essential for responding adverse circumstance and pathogenicity of E. piscicida. Based on the attenuated virulence of TX01 Delta higB, we further investigated its potential as a live vaccine. Vaccination experiment showed that TX01 Delta higB induced effective protection against lethal E. piscicida infection. In addition, we found that antitoxin HigA negatively autoregulated the expression of higBA by binding directly with own promoter, and toxin HigB promoted the regulatory function of HigA. This study provides new insights into the biological activity of type II TA system HigBA in aquatic pathogenic bacteria and contributes to understand the pathogenesis of E. piscicida.

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