文献类型： 外文期刊

作者： Fang, Qing-Jian ¹ ; Han, Yue-Xin ² ; Shi, Yan-Jie ² ; Huang, Hui-Qin ² ; Fang, Zai-Guang ¹ ; Hu, Yong-Hua ² ;

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

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

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

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

关键词： Edwardsiella piscicida; Usp; Adversity resistance; Tilapia; Immune response

期刊名称：FISH & SHELLFISH IMMUNOLOGY （ 影响因子：4.581； 五年影响因子：4.851 ）

ISSN： 1050-4648

年卷期： 2019 年 95 卷

页码：

收录情况： SCI

摘要： Universal stress proteins (Usps) exist ubiquitously in bacteria and other organisms. Usps play an important role in adaptation of bacteria to a variety of environmental stresses. There is increasing evidence that Usps facilitate pathogens to adapt host environment and are involved in pathogenicity. Edwardsiella piscicida (formerly included in E. tarda) is a severe fish pathogen and infects various important economic fish including tilapia (Oreochromis niloticus). In E. piscicida, a number of systems and factors that are involved in stress resistance and pathogenesis were identified. However, the function of Usps in E. piscicida is totally unknown. In this study, we examined the expressions of 13 usp genes in E. piscicida and found that most of these usp genes were up-regulated expression under high temperature, oxidative stress, acid stress, and host serum stress. Particularly, among these usp genes, usp13, exhibited dramatically high expression level upon several stress conditions. To investigate the biological role of usp13, a markerless usp13 in-frame mutant strain, TX01 Delta usp13, was constructed. Compared to the wild type TX01, TX01 Delta usp13 exhibited markedly compromised tolerance to high temperature, hydrogen peroxide, and low pH. Deletion of usp13 significantly retarded bacterial biofilm growth and decreased resistance against serum killing. Pathogenicity analysis showed that the inactivation of usp13 significantly impaired the ability of E. piscicida to invade into host cell and infect host tissue. Introduction of a trans-expressed usp13 gene restored the lost virulence of TX01 Delta usp13. In support of these results, host immune response induced by TX01 and TX01 Delta usp13 was examined, and the results showed reactive oxygen species (ROS) levels in TX01 Delta usp13-infected macrophages were significantly higher than those in TX01-infected cells. The expression level of several cytokines (IL-6, IL-8, IL-10, TNF-alpha, and CC2) in TX01 Delta usp13-infected fish was significantly higher than that in TX01-infected fish. These results suggested that the deletion of usp13 attenuated the ability of bacteria to overcome the host immune response to pathogen infection. Taken together, our study indicated Usp13 of E. piscicida was not only important participant in adversity resistance, but also was essential for E. piscicida pathogenicity and contributed to block host immune response to pathogen infection.