Author/Authors :
Zhang, Junbo Shihezi University - College of Animal Science and Technology, China , Guo, Fei Shihezi University - College of Medicine, China , Chen, Chuangfu Shihezi University - College of Animal Science and Technology, China , Jian, Tong Shihezi University - College of Animal Science and Technology, China , Yin, Shuanghong Shihezi University - College of Medicine, China , Zhang, Hui Shihezi University - College of Animal Science and Technology, China , Wang, Yuanzhi Shihezi University - College of Medicine, China , Li, Zhiqiang Shihezi University - College of Animal Science and Technology, China , Zhang, Ke Shihezi University - College of Animal Science and Technology, China
Abstract :
Brucellosis is a globally distributed zoonotic disease that causes animal and human diseases. Brucella pathogenesis depends on their ability of inhibiting apoptosis and establishes a replicative niche inside host cells. SUMOylation is a major regulator of protein function that is essential for some pathogenic bacteria during infection. However, the relationship between Brucella and SUMOylation remains largely unknown. In our report, we demonstrated that the Brucella melitensis 16M (16M) infection leads to a decrease in the expression of SUMO1 proteins with time-delay, and 16M intracellular replication was inhibited by SUMO-1 overexpression and promoted by SUMO-1 depletion, and 16M-dependent apoptosis and the secretion of gamma interferon and interleukin-6 were induced by SUMO-1 overexpression and restricted by SUMO-1 depletion in the RAW264.7 macrophages. Together, this study shows that SUMO-1 plays an essential role in regulating 16M infection and may help to unravel pathogenic mechanisms of 16M.
Keywords :
Brucella melitensis 16M , Depletion , Overexpression , Survival , Ubiquitin , like protein , SUMO , 1
