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-1 beta expression at both the mRNA and protein levels in the mammary gland epithelial cell-line, MAC-T. IL-1 beta 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-kappa B transcription factors that regulate IL-1 beta gene expression. Among staphylococcal cell-wall components with inflammatory potential, Pam2CSK4 (a representative model for diacylated lipoproteins) enhanced IL-1 beta mRNA expression, while lipoteichoic acid and peptidoglycan did not. Collectively, we suggest that S. aureus-induced IL-1 beta production requires lipid raft formation, activation of MAP kinases, and activation of transcription factors AP-1, CRE, and NF-kappa B. Lipoprotein seems to be a major cell-wall component for the S. aureus-induced IL-1 beta production in bovine mammary gland epithelial cells. (C) 2011 Elsevier Ltd. All rights reserved.