【摘 要】：Brucellosis is a zoonotic pathogen that causes both animal and human diseases. Brucella pathogenesis depends on the bacterial ability of inhibiting apoptosis and establishes a replicative niche inside host cells. The PI3K/Akt pathway regulates various cellular activities (cell growth, survival, and apoptosis). However, the role of the PI3K/Akt pathway in the survival of 16M in RAW264.7 macrophages remains largely unknown. In our report, we demonstrated that the PI3K/Akt pathway was activated by 16M in RAW264.7 macrophages. We found that 16M infection induced the phosphorylation of both Thr-308 and Ser-473 of Akt in a time-dependent manner. This phosphorylation was inhibited by LY in a dose-dependent manner. Inhibition of PI3K/Akt with LY significantly reduced the internalisation and replication of 16M and induced 16M-dependent inhibition of apoptosis, and induced Th1 and proinflammatory responses both in vitro and in vivo and protected mice against 16M infection. These results indicated that the PI3K/Akt pathway plays an important role in 16M survival both in vitro and in vivo, which will help to unravel the pathogenic mechanisms of 16M. (C) 2014 PVJ. All rights reserved