COX-2 mediated crosstalk between Wnt/β-catenin and the NF-κB signaling pathway during inflammatory responses induced by Haemophilus parasuis in PK-15 and NPTr cells.

Haemophilus parasuis infection causes typical acute systemic inflammation in pigs, is characterized by fibrinous polyserositis inflammation, and results in great economic losses to the swine industry worldwide. However, the molecular details of how the host modulates the acute inflammatory response induced by H. parasuis are largely unknown. In previous studies, we found that H. parasuis high-virulence strain SH0165 infection induced the activation of both Wnt/β-catenin and NF-κB signaling in PK-15 and NPTr cells. In this study, we found that the activation of NF-κB, a central hub in inflammatory signaling, was impeded by the Wnt/β-catenin pathway during H. parasuis infection. In contrast, blocking NF-κB activity had no effect on the Wnt/β-catenin pathway during H. parasuis infection. Furthermore, we found that the inhibitory effect of β-catenin on NF-κB activity was mediated by its target gene, pig cyclooxygenase-2 (COX-2). Therefore, we demonstrated that H. parasuis infection activates the canonical Wnt/β-catenin signaling pathway, which leads to decreased NF-κB activity, reducing the acute inflammatory response in pigs. Additionally, the data provide a possible perspective for understanding the anti-inflammatory role of Wnt/β-catenin in pigs during bacterial infection.

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