Staphylococcus aureus mediates pyroptosis in bovine mammary epithelial cell via activation of NLRP3 inflammasome

Veterinary Research

Bo Han¹  Mingchao Liu²  Yongzhen Du³  Xiaozhou Wang³  Zhaoming Li³  Xin Gao³  Yongxia Liu³  Na Geng³  Jianzhu Liu⁴ 

[1] College of Veterinary Medicine, China Agricultural University, 100193, Beijing, China;College of Veterinary Medicine, Hebei Agricultural University, 071001, Baoding, Hebei, China;College of Veterinary Medicine, Shandong Agricultural University, 271018, Tai’an, Shandong, China;College of Veterinary Medicine, Shandong Agricultural University, 271018, Tai’an, Shandong, China;Research Center for Animal Disease Control Engineering, Shandong Agricultural University, 271018, Tai’an, Shandong, China;

关键词: Staphylococcus aureus;    bovine mastitis;    inflammasome;    caspase-1;    pyroptosis;   

DOI  :  10.1186/s13567-022-01027-y

来源: Springer

【 摘 要 】

Cell death and inflammation are intimately linked during mastitis due to Staphylococcus aureus (S. aureus). Pyroptosis, a programmed necrosis triggered by gasdermin protein family, often occurs after inflammatory caspase activation. Many pathogens invade host cells and activate cell-intrinsic death mechanisms, including pyroptosis, apoptosis, and necroptosis. We reported that bovine mammary epithelial cells (MAC-T) respond to S. aureus by NOD-like receptor protein 3 (NLRP3) inflammasome activation through K+ efflux, leading to the recruitment of apoptosis-associated speck-like protein (ASC) and the activation of caspase-1. The activated caspase-1 cleaves gasdermin D (GSDMD) and forms a N-terminal pore forming domain that drives swelling and membrane rupture. Membrane rupture results in the release of the pro-inflammatory cytokines IL-18 and IL-1β, which are activated by caspase-1. Can modulate GSDMD activation by NLRP3-dependent caspase-1 activation and then cause pyroptosis of bovine mammary epithelial cells.

【 授权许可】

CC BY