Staphylococcus aureus induces IL-1β expression through the activation of MAP kinases and AP-1, CRE and NF-κB transcription factors in the bovine mammary gland epithelial cells.

Although mastitis caused by Staphylococcus aureus is a problematic inflammatory disease in lactating cows, the innate immunity to S. aureus in the mammary gland is poorly understood. In the present study, we observed that heat-killed S. aureus (HKS) induced IL-1β expression at both the mRNA and protein levels in the mammary gland epithelial cell-line, MAC-T. IL-1β production was suppressed by inhibitors of lipid rafts, ERK, JNK, and p38 kinases. Furthermore, HKS augmented the activities of the AP-1, CRE, and NF-κB transcription factors that regulate IL-1β gene expression. Among staphylococcal cell-wall components with inflammatory potential, Pam2CSK4 (a representative model for diacylated lipoproteins) enhanced IL-1β mRNA expression, while lipoteichoic acid and peptidoglycan did not. Collectively, we suggest that S. aureus-induced IL-1β production requires lipid raft formation, activation of MAP kinases, and activation of transcription factors AP-1, CRE, and NF-κB. Lipoprotein seems to be a major cell-wall component for the S. aureus-induced IL-1β production in bovine mammary gland epithelial cells.