Influence of platelet-activating factor receptor (PAFR) on Brucella abortus infection: implications for manipulating the phagocytic strategy of B. abortus

BMC Microbiology

Research Article

Jin Ju Lee¹  Moon Her¹  Man Hee Rhee²  Masahisa Watarai³  Hong Hee Chang⁴  Hannah Leah Simborio⁵  Hu Jang Lee⁵  Alisha Wehdnesday Bernardo Reyes⁵  Lauren Togonon Arayan⁵  Wongi Min⁵  Huynh Tan Hop⁵  Suk Kim⁶ 

[1] Animal and Plant Quarantine Agency, 430-757, Anyang, Gyeonggi-do, Republic of Korea;College of Veterinary Medicine, Kyungpook National University, 702-701, Daegu, Republic of Korea;Department of Veterinary Public Health, Faculty of Agriculture, Yamaguchi University, 753-8515, Yamaguchi, Japan;Institute of Agriculture and Life Science, Gyeongsang National University, 660-701, Jinju, Republic of Korea;Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, 660-701, Jinju, Republic of Korea;Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, 660-701, Jinju, Republic of Korea;Institute of Agriculture and Life Science, Gyeongsang National University, 660-701, Jinju, Republic of Korea;

关键词: B. abortus;    Platelet-activating factor receptor;    JAK2;    Phagocytosis;   

DOI  :  10.1186/s12866-016-0685-8

 received in 2015-07-02, accepted in 2016-04-07,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundBrucella abortus is an intracellular pathogen which can infect and persist in host cells through multiple interactions. Above all, its interaction to host cell receptor is important to understand the pathogenic mechanisms of B. abortus. Accordingly, we demonstrated that platelet-activating factor receptor (PAFR) affects host cell response against B. abortus infection.ResultsFirst of all, B. abortus infection to macrophage induces secretion of platelet-activating factor (PAF), which is a PAFR agonist. The stimulation of PAFR by PAF remarkably increases B. abortus uptake into macrophages. It induces Janus kinase 2 (JAK2) and p38α phosphorylation, indicating that PAFR-mediated activation of JAK2 signaling leads to enhanced uptake of B. abortus. Moreover, the dynamics of F-actin polymerization revealed that PAFR-mediated B. abortus uptake is related with the reorganization of F-actin and JAK2. Upon B. abortus phagocytosis, reduced PAFR in the membrane and subsequently increased levels of PAFR colocalization with endosomes were observed which indicate that B. abortus uptake into macrophages allowed PAFR trafficking to endosomes.ConclusionsThis study demonstrated that PAFR has a compelling involvement in B. abortus uptake as a promoter of phagocytosis, which is associated with JAK2 activation. Thus, our findings establish a novel insight into a receptor-related phagocytic mechanism of B. abortus.

【 授权许可】

CC BY   
© Lee et al. 2016