Journal
VETERINARY RESEARCH
Volume 53, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s13567-022-01027-y
Keywords
Staphylococcus aureus; bovine mastitis; inflammasome; caspase-1; pyroptosis
Categories
Funding
- National Natural Science Foundation of China [31802259, 31872535]
- Shandong Key RD Program [2019GNC106141]
- Shandong Natural Science Foundation of China [ZR2018MC027]
- China Postdoctoral Science Foundation [2018M632704, 2019T120601]
- Funds of Shandong Double Tops Program
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Cell death and inflammation are closely linked during mastitis caused by Staphylococcus aureus. Bovine mammary epithelial cells respond to S. aureus by NLRP3 inflammasome activation, leading to cell apoptosis and pyroptosis. This cell death process is associated with caspase-1 activation.
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-1 beta, 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.
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