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Activation of the PI3K/Akt Pathway is Essential for the Survival of Brucella melitensis 16M In Vitro and In Vivo
Junbo Zhang1,2§, Shuanghong Yin1,3§, Fei Guo4, Zhiqing Li1, Chuangfu Chen1* and  Hui Zhang1
1College of Animal Science and Technology, Shihezi University, Shihezi 832003, China; 2College of Biology, Agriculture and Forestry, Tongren University, Tongren, 554300, Guizhou, China ;3College of Material and Chemical Engineering, Tongren University, Tongren, 554300, Guizhou, China ;4College of Medicine, Shihezi University, Shihezi, 832003, China; *Corresponding author:


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.

Key words: Brucella melitensis 16M, Cell apoptosis, PI3K/Akt pathway, Survival


ISSN 0253-8318 (Print)
ISSN 2074-7764 (Online)