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Background   Brucella 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.    Results  First 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.    Conclusions  This 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 .    Electronic supplementary material  The online version of this article (doi:10.1186/s12866-016-0685-8) contains supplementary material, which is available to authorized users.

bmc microbiology

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