Overexpression of Cu-Zn SOD in  Brucella abortus  suppresses bacterial intracellular replication via down-regulation of Sar1 activity

Xiaofeng Liu; Mi Zhou; Yanling Yang; Jing wu; Qisheng Peng

doi:10.18632/oncotarget.24073

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Research Papers: Immunology:

Overexpression of Cu-Zn SOD in Brucella abortus suppresses bacterial intracellular replication via down-regulation of Sar1 activity

Xiaofeng Liu, Mi Zhou, Yanling Yang, Jing wu _ and Qisheng Peng

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Oncotarget. 2018; 9:9596-9607. https://doi.org/10.18632/oncotarget.24073

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Abstract

Xiaofeng Liu2, Mi Zhou3, Yanling Yang4, Jing Wu5 and Qisheng Peng1

1Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis, Jilin University, Changchun 130062, China

2Tumor Hospital of Jilin Province, Changchun 130021, China

3Changchun Medical College, Changchun 130031, China

4Institute of Special Wild Animal and Plant Science, Chinese Academy of Agricultural Sciences, Changchun 130122, China

5School of Nursing, Gansu University of Chinese Medicine, Lanzhou 730000, China

Correspondence to:

Qisheng Peng, email: [email protected]

Keywords: Brucella; SOD; Sar1

Received: June 20, 2017 Accepted: November 15, 2017 Published: January 10, 2018

ABSTRACT

Brucella Cu-Zn superoxide dismutase (Cu-Zn SOD) is a periplasmic protein, and immunization of mice with recombinant Cu-Zn SOD protein confers protection against Brucella abortus infection. However, the role of Cu-Zn SOD during the process of Brucella infection remains unknown. Here, we report that Cu-Zn SOD is secreted into culture medium and is translocated into host cells independent of type IV secretion systems (T4SS). Furthermore, co-immunoprecipitation and immunofluorescence studies reveal that Brucella abortus Cu-Zn SOD interacts with the small GTPase Sar1. Overexpression of Cu-Zn SOD in Brucella abortus inhibits bacterial intracellular growth by abolishing Sar1 activity in a manner independent of reactive oxygen species (ROS) production.

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Research Papers: Immunology:

Overexpression of Cu-Zn SOD in Brucella abortus suppresses bacterial intracellular replication via down-regulation of Sar1 activity

Abstract