The role of jak2/stat3 signaling pathway regulation in macrophage apoptosis during brucella m5-90 infection

Brucellosis is serious zoonotic disease affecting both animals and humans. Brucella inhibits the apoptosis of host macrophages. And the JAK2/STAT3 pathway regulates various cellular physiological activities. However, the association between Brucella-mediated inhibition of macrophage apoptosis and regulation of the JAK2/STAT3 pathway is unclear. In the current study, We tested the the activation of JAK2/ STAT3 pathway and evaluated its function during Brucella M5-90 infection in cells. The result was found that infection with Brucella M5-90 activated the JAK2/STAT3 pathway and induced phosphorylation of both JAK2 and STAT3 in a time-dependent manner. JAK2 and STAT3 phosphorylation were inhibited by AG490 in a dose-dependent manner. Inhibition of the JAK2/STAT3 pathway with AG490 significantly induced proinflammatory responses, macrophage apoptosis at the transcriptional and protein levels, as well as intracellular survival and replication of Brucella M5-90. This study indicates that the JAK2/STAT3 pathway plays a major role in macrophage apoptosis induced by infection with Brucella M5-90. In addition, TNF-α plays a major role in the regulation of the JAK2/STAT6 pathway during Brucella M5-90 infection. The above information may help to unravel the pathogenic mechanism of Brucella infection.