Abstract
In this study, animal experimentation verified that the canonical Wnt/β-catenin signaling pathway was activated under a reduced activity of p-β-catenin (Ser33/37/Thr41) and an increased accumulation of β-catenin in the lungs and kidneys of pigs infected with a highly virulent strain of H. parasuis. In PK-15 and NPTr cells, it was also confirmed that infection with a high-virulence strain of H. parasuis induced cytoplasmic accumulation and nuclear translocation of β-catenin. H. parasuis infection caused a sharp degradation of E-cadherin and an increase of the epithelial cell monolayer permeability, as well as a broken interaction between β-catenin and E-cadherin dependent on Wnt/β-catenin signaling pathway. Moreover, Wnt/β-catenin signaling pathway also contributed to the initiation of epithelial-mesenchymal transition (EMT) during high-virulence strain of H. parasuis infection with expression changes of epithelial/mesenchymal markers, increased migratory capabilities as well as the morphologically spindle-like switch in PK-15 and NPTr cells. Therefore, we originally speculated that H. parasuis infection activates the canonical Wnt/β-catenin signaling pathway leading to a disruption of the epithelial barrier, altering cell structure and increasing cell migration, which results in severe acute systemic infection characterized by fibrinous polyserositis during H. parasuis infection.
Highlights
Haemophilus parasuis is the etiological agent of Glässer’s disease, an important bacterial disease in swine worldwide, which causes serious economic loss to the global pig industry (Olvera et al, 2007; Frandoloso et al, 2012)
To investigate the role of the Wnt/β-catenin signaling pathway in vivo after H. parasuis infection, we examined the expression of β-catenin in kidney and lung tissues of pigs following infection with the high-virulence H. parasuis strain SH0165 and the nonvirulent strain H. parasuis HN0001
These results indicated that H. parasuis infection with the high-virulence strain, but not the non-virulent strain, activated the Wnt/β-catenin signaling pathway in vivo
Summary
Haemophilus parasuis is the etiological agent of Glässer’s disease, an important bacterial disease in swine worldwide, which causes serious economic loss to the global pig industry (Olvera et al, 2007; Frandoloso et al, 2012). The sudden death caused by H. parasuis is a typical acute systemic inflammation with massive fibrin exudates in the pleuroperitoneal cavity as well as membranes (Nedbalcova et al, 2006). We selected two epithelial cells as models, kidney-15 (PK-15) and Newborn pig tracheal (NPTr) cells. Previous studies demonstrate that PK15 cells are suitable models for studying H. parasuis-induced inflammation and immunity (Chen et al, 2012, 2015a,b). NPTr cells are involved in the initial colonization of H. parasuis (Bouchet et al, 2009), and are suitable for exploring its pathogenesis
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