Activation of JNK/MAPK pathway is related to the disruption of TJ and increased-permeability of tracheal epithelial barrier. A Western blotting analysis of p38, ERK and JNK phosphorylation in PCV2-infected STEC. STEC were infected with PCV2 for 36 h or 48 h. Phosphorylation of JNK was detected in the process of PCV2 infection. B Western blotting analysis of ZO-1 and occludin in PCV2-infected STEC treated with JNK inhibitor SP600125. Band intensities relative to control were analyzed. Compared with the PCV2-infected cells, the disruption of ZO-1 and occludin were alleviated through inhibition of JNK activation. CT, the control group. P, the PCV2 infection group. C Measurement of paracellular permeability. PCV2 infection increased the permeability of the epithelial barrier, which can be partially offset by JNK inhibitor. The results are described as mean ± SD of three independent experiments. Significant differences in (B) and (C) were determined using one-way ANOVA analysis. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant. D Immunofluorescence staining of ZO-1 and occludin in STEC. Scale bar, 50 μm. The infection time of PCV2 was 48 h.