High-mobility group box 1
protein (
HMGB1) shows endogenous damage-associated molecular patterns (DAMPs) and is also an early warning
protein that activates the body's innate immune system. Here, the full-length coding sequence of
HMGB1 was cloned from the spleen of Cherry Valley duck and analyzed. We find that duck
HMGB1(duHMGB1) is mostly located in the nucleus of duck embryo fibroblast (
DEF) cells under normal conditions but released into the cytoplasm after
lipopolysaccharide (LPS) stimulation. Knocking-down or overexpressing duHMGB1 had no effect on the baseline apoptosis rate of
DEF cells. However, overexpression increased weakly apoptosis after LPS activation. In addition, overexpression strongly activated the IFN-I/IRF7 signaling pathway in
DEF cells and significantly increased the transcriptional level of numerous
pattern recognition receptors (
PRRs), pro-inflammatory
cytokines (IL-6, TNF-α), IFNs and
antiviral molecules (OAS, PKR, Mx) starting from 48 h post-transfection. Overexpression of duHMGB1 strongly impacted duck virus replication, either by inhibiting it from the first stage of
infection for novel duck reovirus (NDRV) and at late stage for duck Tembusu virus (DTMUV) or duck
plague virus (DPV), or promoting replication at early stage for DTMUV and DPV
infection. Importantly, data from duHMGB1 overexpression and knockdown experiments, time-dependent
DEF cells transcriptional immune responses suggest that duHMGB1 and RIG-I receptor might cooperate to promote the expression of
antiviral proteins after NDRV
infection, as a potential mechanism of duHMGB1-mediated
antiviral activity.