An underlying mechanism of bovine mastitis: PGE₂ regulates <i>Staphylococcus aureus</i>-induced inflammatory response through TLR2, TLR4, and NLRP3 in macrophages.

ABSTRACT: Staphylococcus aureus (S. aureus) evades host immunity by modulating macrophage functions, including immune regulation and phagocytosis, ultimately contributing to bovine mastitis. This study aimed to elucidate the molecular mechanisms of S. aureus-induced bovine mastitis from both host and pathogen perspectives, focusing on prostaglandin E₂ (PGE₂) as a key regulator. During bovine mastitis, macrophages were recruited into the mammary gland with elevated inflammatory mediators. S. aureus lipoproteins amplified inflammation by activating MAPK and NF-κB pathways via TLR2, TLR4, and NLRP3, leading to elevated secretion of mediators, including PGE₂, in bBMMs. Inhibition of TLR2, TLR4, or NLRP3 decreased COX-2 and mPGES-1 expre

SUBMITTER: Gong Z 

PROVIDER: S-EPMC12818336 | biostudies-literature | 2026 Dec

REPOSITORIES: biostudies-literature