Abstract: To explore the influence of Staphylococcus aureus on IFN-α production and IFN-α mRNA expression in microglia cells. IFN-α released into the culture medium and TBK1/IRF3 signaling of BV2 cells were detected after BV2 cells were infected with S. aureus. TBK1/IRF3 pathway activation and IFN-α levels were detected after S. aureus infected BV2 cells which were treated by BX-795, amlexanox, IMD-0354 inhibitors, respectively. The results showed that IFN-α transcriptional levels increased from 3 to 12 hours post infection, and IFN-α release was enhanced from 6 to 12 hours post infection in a dose-dependent manner. TBK1 and IRF3 were not affected at both the mRNA and protein levels, but their phosphorylation was triggered from 1 to 12 hours, indicating that S. aureus infection activated TBK1/IRF3 pathway. IRF3 phosphorylation and IFN-α were attenuated in the presence of BX-795, amlexanox or IMD-0354, indicating that TBK1 and NF-κB were involved in S. aureus-induced IFN-α release. Collectively, S. aureus infection leads to TBK1-and NF-κB-dependent IFN-α production. It provides potential targets and theoretical basis for clinical prevention and treatment of S. aureus infection in the central nervous system.

Key words: Staphylococcus aureus, BV2, IFN-α, TBK1, IRF3