Bacterial pathogens have evolved various mechanisms to modulate host immune responses for successful infection.In this study,RNAsequencing technology was used to analyze the responses of human monocytes THP1 to Yersinia pestis infection.Over 6000 genes were differentially expressed over the 12 h infection.Kinetic responses of pathogen recognition receptor signaling pathways,apoptosis,antigen processing,and presentation pathway and coagulation system were analyzed in detail.Among them,RIG-I-like receptor(RLR) signaling pathway,which was established for antiviral defense,was significantly affected.Mice lacking MAVS,the adaptor of the RLR signahng pathway,were less sensitive to infection and exhibited lower IFN-P production,higher Thl-type cytokines IFN-y and IL-12 production,and lower Th2-type cytokines EL-4 and IL-13 production in the serum compared with wild-type mice.Moreover,infection of pathogenic bacteria other than Y.pestis also altered the expression of the RLR pathway,suggesting that the response of RLR pathway to bacterial infection is a universal mechanism. Bacterial pathogens have evolved various mechanisms to modulate host immune responses for successful infection. In this study, RNAsequencing technology was used to analyze the responses of human monocytes THP1 to Yersinia pestis infection. Over 6000 genes were differentially expressed over the 12 h infection. Kittic responses of pathogen recognition receptor signaling pathways, apoptosis, antigen processing, and presentation pathway and coagulation system were analyzed in detail. Among them, RIG-I-like receptor (RLR) signaling pathway, which was established for antiviral defense, was significantly affected. Mice lacking MAVS, the adapter of the RLR signaling pathway, were less sensitive to infection and exploring lower IFN-P production, higher Thl-type cytokines IFN- and IL-12 production, and lower Th2-type cytokines EL- 4 and IL- 13 production in the serum compared with wild-type mice. Moreover, infection of pathogenic bacteria other than Y. pestis also altered the expression of the RLR pathway, suggesting that the response of RLR pathway to bacterial infection is a universal mechanism.