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

• Published in: Veterinary research (Paris) 2022-02, Vol.53 (1), p.10-10, Article 10
• Main Authors: Wang, Xiaozhou, Liu, Mingchao, Geng, Na, Du, Yongzhen, Li, Zhaoming, Gao, Xin, Han, Bo, Liu, Jianzhu, Liu, Yongxia
• Format: Article
• Language: English
• Subjects: Animals; Antibodies; Apoptosis; Bacteria; Bacterial infections; bovine mastitis; caspase-1; Cattle; Cell culture; Cytokines; Cytotoxicity; Dairy industry; Epithelial Cells - metabolism; Female; inflammasome; Inflammasomes - metabolism; Inflammation; Interleukin-1beta - metabolism; Lymphocytes; Membranes; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism; NLR Proteins; Peptides; Plasma; Pyroptosis; Staphylococcus aureus; Staphylococcus aureus - metabolism; Staphylococcus aureus infections; Staphylococcus infections
• ISSN: 1297-9716; 0928-4249; 1297-9716
• DOI: 10.1186/s13567-022-01027-y

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.