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Received: Revised: Accepted: Published online: August 15, 2017 March 10, 2018 March 12, 2018 April 24, 2018 Brucellosis is an important zoonotic pathogen of worldwide distribution that causes disease in both humans and animals. Brucella can weaken the immune ability of host cells and its pathogenesis depends on its ability to replicate intracellularly and inhibit host cell apoptosis. The JAK2/STAT3 pathway is known to regulate various biological functions, to include cell differentiation, cell death, and apoptosis. However, the role of this pathway in the survival of virulent or low virulent Brucella strains in macrophages remains largely uncharacterized. In this study, the JAK2/STAT3 pathway was found to be activated by both smooth Brucella abortus 2308 (B. abortus; virulent) and rough B. abortus RB51 (low virulent), but only B. abortus RB51 significantly induced JAK2 and STAT3 phosphorylation in a timedependent manner. Furthermore, in B. abortus RB51, JAK2/STAT3 phosphorylation was inhibited by AG490 (inhibitor of JAK2/STAT3 pathway) in a dosedependent manner and B. abortus RB51-mediated apoptosis and cytokines (IL-6, TNF-α) expression were also inhibited. These findings suggest that JAK2/ STAT3 pathway is important to intercellular survival during a B. abortus RB51 infection, but does not appear to play an apparent role in B. abortus 2308 survival.

Effects of JAK2 / STAT3 Signaling Pathway Activation on Intracellular Survival of Brucella