한빛사 논문
경상대학교 수의과대학
Abstract
Alisha Wehdnesday Bernardo Reyesa,1, Son Hai Vua,1, Tran Xuan Ngoc Huya, WonGi Mina, Hu Jang Leea, Hong Hee Changa, John Hwa Leeb, Suk Kima,*
a Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju, 52828, Republic of Korea
b College of Veterinary Medicine, Chonbuk National University, Iksan, 54596, Republic of Korea
*Corresponding author : Suk Kim
1These authors contributed equally in this work.
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.
Keywords : Adora2b; Brucellaabortuscytokines; macrophages; spleen
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