Classical swine fever virus failed to activate nuclear factor-kappa b signaling pathway both in vitro and in vivo
Classical swine fever virus (CSFV) is the cause of CSF which is a severe disease of pigs, leading to heavy economic losses in many regions of the world. Nuclear factor-kappa B (NF-ÎºB) is a critical regulator of innate and adaptive immunity, and commonly activated upon viral infection. In our previous study, we found that CSFV could suppress the maturation and modulate the functions of monocyte-derived dendritic cells (Mo-DCs) without activating NF-ÎºB pathway. To further prove the effects of CSFV on the NF-ÎºB signaling pathway, we investigated the activity of NF-ÎºB after CSFV infection in vivo and in vitro.
Attenuated Thiverval strain and virulent wild-type GXW-07 strain were used as challenge viruses in this study. Porcine kidney 15 (PK-15) cells were cultured in vitro and peripheral blood mononuclear cells (PBMCs) were isolated from the blood of CSFV-infected pigs. DNA binding of NF-ÎºB was measured by electrophoretic mobility shift assays (EMSA), NF-ÎºB p65 translocation was detected using immunofluorescent staining, and p65/RelA and IÎºBÎ± expression was measured by Western Blotting.
Infection of cells with CSFV in vitro and in vivo showed that compared with tumor necrosis factor alpha (TNF-Î±) stimulated cells, there was no distinct DNA binding band of NF-ÎºB, and no significant translocation of p65/ RelA from the cytoplasm to the nucleus was observed, which might have been due to the apparent lack of IkBa degradation.
CSFV infection had no effect on the NF-ÎºB signaling pathway, indicating that CSFV could evade host activation of NF-ÎºB during infection.
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Article made possible through the contribution of Li-Jun Chen et al. Biomed Central