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

• Published in: BMC veterinary research Vol. 17; no. 1; p. 114
• Main Authors: Shan, Chunlan, Miao, Shushu, Liu, Chaoying, Zhang, Bo, Zhao, Weiwei, Wang, Hao, Yang, Wei, Cha, Jinlong, Zhao, Ru, Xiao, Peng, Gao, Hong
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 07.03.2021; BioMed Central; BMC
• Subjects: Analysis; Apoptosis; Caspase-1; Cell membranes; Cytokines; E coli; Escherichia coli; Genes; Health aspects; HPI; IL-1β; Infections; Inflammatory diseases; Interleukin 18; L-Lactate dehydrogenase; Lactic acid; Lipopolysaccharides; Macrophage; Macrophages; Membrane permeability; Pathogenic E. coli; Pathogenicity; Permeability; Propidium iodide; Proteins; Pyroptosis; Signal transduction; Swine; Virulence; China; HPI; Pyroptosis; Pathogenic E. coli; Caspase-1; Macrophage
• ISSN: 1746-6148; 1746-6148
• DOI: 10.1186/s12917-021-02824-x

Pyroptosis 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. After 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. Our 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.