Protective effects of chlorogenic acid on inflammatory responses induced by Staphylococcus aureus and milk protein synthesis in bovine mammary epithelial cells

Staphylococcus aureus (S. aureus) is a major mastitis-causing pathogen in dairy cows. Dairy cows with mastitis suffer from a decrease in milk yield and protein content. Chlorogenic acid (CGA) is a natural product with anti-inflammatory effects. In this study, we examined the function and mechanism of CGA with regard to its anti-inflammatory effects and evaluated its protective function in milk protein synthesis in bovine mammary epithelial cells (BMECs). BMECs were cultured with and without infection by S. aureus and CGA, and extracel-lular inflammatory cytokines and amino acids in the medium and milk proteins were determined by ELISA. The function of IL-10RA in anti-inflammatory processes and of SF-1 in milk protein synthesis was assessed by gene silencing. The activity of mTORC1, NF-kappa B, and STAT5 was examined by western blot. S. aureus caused intra-cellular infection and upregulated TNF-alpha, IL-1 beta, IL-6, and IL-8, whereas uptake of amino acids and milk protein synthesis were suppressed. CGA mitigated the S. aureus-induced inflammatory response and milk protein syn-thesis in vitro and in vivo. CGA alleviated S. aureus-induced inhibition of mTORC1 and STAT5 and upregulated IL -10 and IL-10RA. In addition, SF-1 was predicted to be a transcription factor of the milk protein-encoding genes alpha-LA, beta-LG, and CSN2. S. aureus downregulated SF-1 and CGA reversed the decline in milk protein synthesis due to SF-1 knockdown. Thus, CGA mitigates the inflammatory response that is induced by S. aureus and protects the uptake of amino acids and milk protein synthesis in BMECs.

Automated summary

This study found that chlorogenic acid (CGA) mitigates the inflammatory response caused by Staphylococcus aureus, protects milk protein synthesis, and improves amino acid uptake in bovine mammary epithelial cells (BMECs). CGA regulates the activity of mTORC1 and STAT5, upregulates IL-10 and IL-10RA, and reverses the inhibition of milk protein synthesis caused by Staphylococcus aureus.