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- W3000682859 abstract "Brucella as a stealthy intracellular pathogen avoids activation of innate immune response. Here we investigated the contribution of an adenosine receptor, Adora2b, during Brucella infection in professional phagocyte RAW 264.7 cells and in a murine model. Adora2b-deficient cells showed attenuated Brucella internalization and intracellular survival with enhanced release of IL-6, TNF-α, IL-12 and MCP-1. In addition, blockade of Adora2b using MRS 1754 treatment in mice resulted in increased total weight of the spleens but suppressed bacterial burden in these organs accompanied by elevated levels of IL-6, IFN-γ, TNF-α, IL-12 and MCP-1, while reduced IL-10. Overall, we proposed that the Adora2b participates in the successful phagocytic pathway and intracellular survival of Brucella in RAW 264.7 cells, and could be a potential therapeutic target for the treatment of acute brucellosis in animals." @default.
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- W3000682859 date "2020-03-01" @default.
- W3000682859 modified "2023-10-17" @default.
- W3000682859 title "Adenosine receptor Adora2b antagonism attenuates Brucella abortus 544 infection in professional phagocyte RAW 264.7 cells and BALB/c mice" @default.
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- W3000682859 doi "https://doi.org/10.1016/j.vetmic.2020.108586" @default.
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