Porcine parvovirus infection activates inflammatory cytokine production through Toll-like receptor 9 and NF-κB signaling pathways in porcine kidney cells

•This review provides an new insights into the molecular pathogenesis of PPV-induced inflammation.•It discusses the regulation of inflammatory cytokines after PPV infected PK-15 cells.•It discusses NF-κB mediates PPV-induced IL-6, IL-12 and TNF-α in PK-15 cells.•It discusses PPV induced activation of NF-κB signaling pathways mediated by TLR9 and via MyD88 pathway.•It discusses TLR9 were require for induction of IL-6 by PPV in PK-15 cells. Porcine parvovirus virus (PPV) is an animal virus that has caused high economic losses for the swine industry worldwide. Previous studies demonstrated that PPV infection induced significant production of interleukin 6 (IL-6) in vitro and in vivo. However, the inflammatory cytokines and specific signaling pathways induced during PPV infection remain largely unknown. In the present study, we analyzed the expression levels of IL-6 in PPV-infected porcine kidney 15 (PK-15) and the results showed that PPV infection induced the increase of IL-6 mRNA expression in a dose-dependent manner. We also detected the expression of toll-like receptor 9 (TLR9) signaling proteins in the mRNA expressing level, when compared with the control group, the TLR9 expression in mRNA level increased at 24h in PK-15 cells after PPV infection and reached the peak level at 48h. In addition, the transcript profile of nuclear factor kappa B (NF-κB) signal pathway relating genes (MyD88, IRAK1, TRAF6, TAK1α, IκBκB and NF-κB) expression levels increased at different times. Furthermore, to verify the IL-6 expression was specific with the TLR9 expression and then by activating the NF-κB signal pathway, TLR9 and NF-κB specific inhibitors were applied during PPV infection, separately, the result indicated that the expression of IL-6 was decreased after inhibitor treatment. Taken together, PPV infection significantly induced IL-6 expression and this induction depended on NF-κB activation and TLR9 signaling pathways in PK-15 cell.