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Host Prdx6 contributing to the intracellular survival of Brucella suis S2 strain

Background Brucellosis is a worldwide zoonotic infectious disease that is transmitted in various ways and causes great harm to humans and animals. The brucellosis pathogen is Brucella, which mainly resides in macrophage cells and survives and replicates in host cells. However, the mechanisms underly...

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Bibliographic Details
Published in:BMC Veterinary Research 2019, Vol.15 (1)
Main Authors: Wang, Lu-Lu, Chen, Xiao-Feng, Hu, Pan, Lu, Shi-Ying, Fu, Bao-Quan, Li, Yan-Song, Zhai, Fei-Fei, Ju, Dan-Di, Zhang, Shi-Jun, Shui, Yi-Ming, Chang, Jiang, Ma, Xiao-Long, Su, Bing, Zhou, Yu, Liu, Zeng-Shan, Ren, Hong-Lin
Format: Report
Language:English
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Summary:Background Brucellosis is a worldwide zoonotic infectious disease that is transmitted in various ways and causes great harm to humans and animals. The brucellosis pathogen is Brucella, which mainly resides in macrophage cells and survives and replicates in host cells. However, the mechanisms underlying Brucella survival in macrophage cells have not been thoroughly elucidated to date. Peroxiredoxin 6 (Prdx6) is a bifunctional protein that shows not only GSH peroxidase activity but also phospholipase A2 activity and plays important roles in combating oxidative damage and regulating apoptosis. Results Recombinant mouse (Mus musculus) Prdx6 (MmPrdx6) was expressed and purified, and monoclonal antibodies against MmPrdx6 were prepared. Using the Brucella suis S2 strain to infect RAW264.7 murine macrophages, the level of intracellular Prdx6 expression first decreased and later increased following infection. Overexpressing Prdx6 in macrophages resulted in an increase in B. suis S2 strain levels in RAW264.7 cells, while knocking down Prdx6 reduced the S2 levels in cells. Conclusions Host Prdx6 can increase the intracellular survival of B. suis S2 strain and plays a role in Brucella infection. Keywords: Host, Prdx6, Brucella, Macrophage, Intracellular survival
ISSN:1746-6148
1746-6148
DOI:10.1186/s12917-019-2049-8