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Background  The tick-borne intracellular pathogen,  Anaplasma phagocytophilum  (Rickettsiales: Anaplasmataceae) causes human granulocytic anaplasmosis after infection of polymorphonuclear leucocytes. The human Sp110 gene is a member of the nuclear body (NB) components that functions as a nuclear hormone receptor transcriptional coactivator and plays an important role in immunoprotective mechanisms against pathogens in humans. In this research, we hypothesized that Sp110 may be involved in the infection of human promyelocytic HL-60 cells with  A. phagocytophilum .    Methods  The human Sp110 and  A. phagocytophilum msp4  mRNA levels were evaluated by real-time RT-PCR in infected human HL-60 cells sampled at 0, 12, 24, 48, 72 and 96 hours post-infection. The effect of Sp110 expression on  A. phagocytophilum  infection was determined by RNA interference (RNAi). The expression of Sp110 was silenced in HL-60 cells by RNAi using pre-designed siRNAs using the Nucleofector 96-well shuttle system (Amaxa Biosystems, Gaithersburg, MD, USA). The  A. phagocytophilum  infection levels were evaluated in HL-60 cells after RNAi by real-time PCR of  msp4  and normalizing against human  Alu  sequences.    Results  While Sp110 mRNA levels increased concurrently with  A. phagocytophilum  infections in HL-60 cells, the silencing of Sp110 expression by RNA interference resulted in decreased infection levels.    Conclusion  These results demonstrated that Sp110 expression is required for  A. phagocytophilum  infection and multiplication in HL-60 cells, and suggest a previously undescribed mechanism by which  A. phagocytophilum  modulates Sp110 mRNA levels to facilitate establishment of infection of human HL-60 cells.

Sp110 transcription is induced and required by Anaplasma phagocytophilumfor infection of human promyelocytic cells