MyD88 and TLR9 are required for early control of Brucella ovis infection in mice.

Abstract Brucella ovis is an important cause of epididymitis in rams, which results in impaired fertility and economic losses. This study demonstrated the role of TLR during the acute phase of infection in the mouse model. C57BL/6 wild type and TLR2 −/− , TLR4 −/− , TLR9 −/− , and MyD88 −/− mice were infected with B. ovis and bacteriology, histopathology, and pro-inflammatory gene expression were evaluated at 7 days post-infection. MyD88 −/− mice had higher bacterial loads in the spleen when compared to wild type mice. This enhanced susceptibility was associated with decreased inflammatory response in the liver. TLR9 −/− mice also had higher bacterial loads when compared to wild type mice, but, surprisingly, they developed stronger inflammatory response. TLR2 −/− and TLR4 −/− mice were as susceptible as wild type mice to B. ovis infection. Therefore, MyD88 and TLR9 are required for controlling B. ovis multiplication during the early stages of infection.