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 will help to unravel pathogenic mechanisms of 16M.

Key words: Brucella melitensis 16M, Depletion, Overexpression, Survival, Ubiquitin-like protein SUMO-1