1College
of Animal Science and Technology, Shihezi University, Shihezi
832000, China
2College of Biology, Agriculture and Forestry, Tongren
University, Tongren, 554300, Guizhou, China
*Corresponding author:
chuangfu_chen@163.com
Abstract
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 time-dependent manner. Furthermore, in B. abortus
RB51, JAK2/STAT3 phosphory-lation was inhibited by AG490 (inhibitor of
JAK2/STAT3 pathway) in a dose-dependent 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.
To Cite This Article:
Yi J, Wang Y, Zhang J, Xu J, Li T and Chen C, 2018. Effects of JAK2 / STAT3 Signaling Pathway Activation
on Intracellular Survival of Brucella. Pak Vet J, 38(2): 153-158.
http://dx.doi.org/10.29261/pakvetj/2018.048