bay-60-6583 and Brucellosis

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.

Topics: Acetamides; Adenosine A2 Receptor Agonists; Adenosine A2 Receptor Antagonists; Aminopyridines; Animals; Brucella abortus; Brucellosis; Cytokines; Female; Immunity, Innate; Macrophages; Mice; Mice, Inbred BALB C; Phagocytosis; Purines; RAW 264.7 Cells; Receptor, Adenosine A2B; Signal Transduction