Haemophilus parasuis Infection Disrupts Adherens Junctions and Initializes EMT Dependent on Canonical Wnt/β-Catenin Signaling Pathway

Frontiers in Cellular and Infection Microbiology

Xueying Hu²  Hufeng Zhou³  Hui Jin⁵  Yangjie Li⁵  Rui Luo⁵  Rongrong He⁵  Dingren Bi⁵  Rui Zhou⁵  Kexin Hua⁵  Yushan Chen⁶ 

[1] Brain and Cognition Research Institute, Wuhan University of Science and Technology, Wuhan, China;College of Animal Medicine, Huazhong Agricultural University, Wuhan, China;Department of Immunology and Microbiology, Harvard Medical School, Boston, MA, United States;Department of Medicine, Brigham and Women's Hospital, Boston, MA, United States;Hubei Provincial Key Laboratory of Preventive Veterinary Medicine, Huazhong Agricultural University, Wuhan, China;Key Laboratory of Occupational Hazard Identification and Control in Hubei Province, Wuhan University of Science and Technology, Wuhan, China;State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China;

关键词: Haemophilus parasuis;    Wnt/β-catenin;    E-cadherin;    adherens junctions;    EMT;   

DOI  :  10.3389/fcimb.2018.00324

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown