Porcine parvovirus induces activation of NF-κB signaling pathways in PK-15 cells mediated by toll-like receptors

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Abstract

Porcine parvovirus (PPV) is a pathogenic factor that primarily induces severe reproductive failure of pregnant swine, which results in extensive losses to the swine industry worldwide. In this study, a potential mechanism of PPV-induced activation of the nuclear transcription factor-kappaB (NF-κB) by infection in porcine kidney cells (PK-15) was elucidated for the first time. The subcellular localization of p65 analyzed by immunofluorescence assay (IFA) showed that PPV infection induced p65 translocation from the cytoplasm to the nucleus. p65 phosphorylation was detected in PK-15 cells with progression of PPV infection. NF-κB-regulated gene expression was enhanced in a viral dose-dependent manner using the NF-κB luciferase reporter assay system. Furthermore, PPV-induced NF-κB activation was closely related to the inhibitory kappa B alpha (IκBα) degradation. Treatment with a NF-κB-specific inhibitor demonstrated that the production of PPV progeny viruses was enhanced to some extent. In addition, these results demonstrated that the adapter molecule TIR domain-containing adapter inducing IFN-β (TRIF) and myeloid differentiation primary-response protein 88 (MyD88)-dependent signaling pathways were involved in PPV-induced NF-κB activation. Together, these results provide evidence that the toll-like receptor (TLR) pathway participates in recognition of PPV and induction of NF-κB activation, and add to understanding of the molecular mechanisms underlying PPV infection.

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