Induction of macrophage pyroptosis-related factors by pathogenic E. coli high pathogenicity island (HPI) in Yunnan Saba pigs

BMC Veterinary Research

Chunlan Shan¹  Chaoying Liu¹  Bo Zhang¹  Weiwei Zhao²  Wei Yang³  Peng Xiao³  Hong Gao³  Hao Wang³  Ru Zhao³  Shushu Miao³  Jinlong Cha³ 

[1] College of Animal Science and Technology, Yunnan Agricultural University, 650201, Kunming, China;College of Food Science and Technology, Yunnan Agricultural University, 650201, Kunming, China;College of Veterinary Medicine, Yunnan Agricultural University, 650201, Kunming, China;

关键词: E. coli;    HPI;    Macrophage;    Pyroptosis;    Caspase-1;   

DOI  :  10.1186/s12917-021-02824-x

来源: Springer

【 摘 要 】

BackgroundPyroptosis plays a pivotal role in the pathogenesis of many inflammatory diseases. The molecular mechanism by which pyroptosis is induced in macrophages following infection with pathogenic E. coli high pathogenicity island (HPI) will be evaluated in our study.ResultsAfter infection with the HPI+/HPI− strains and LPS, decreased macrophage cell membrane permeability and integrity were demonstrated with propidium iodide (PI) staining and the lactate dehydrogenase (LDH) assay. HPI+/HPI−-infection was accompanied by upregulated expression levels of NLRP3, ASC, caspase-1, IL-1β, IL-18 and GSDMD, with significantly higher levels detected in the HPI+ group compared to those in the HPI− group (P < 0.01 or P < 0.05). HPI+ strain is more pathogenic than HPI− strain.ConclusionOur findings indicate that pathogenic E. coli HPI infection of Saba pigs causes pyroptosis of macrophages characterized by upregulated expression of pyroptosis key factors in the NLRP3/ASC/caspase-1 signaling pathway, direct cell membrane pore formation, and secretion of the inflammatory factor IL-1β and IL-18 downstream of NLRP3 and caspase-1 activation to enhance the inflammatory response.

【 授权许可】

CC BY