Butyrate Protects against γ-d-Glutamyl-meso-diaminopimelic Acid-Induced Inflammatory Response and Tight Junction Disruption through Histone Deacetylase 3 Inhibition in Bovine Mammary Epithelial Cells

The present study was conducted to evaluate the regulatory actions and underlying mechanisms of butyrate on the inflammatory response and tight junction (TJ) disruption in bovine mammary epithelial cells (BMECs). Results showed that butyrate declined histone deacetylase 3 (HDAC3) expression, blocked NF-kappa B activation, and thus suppressed inflammatory cytokine production in gamma-d-glutamyl-meso-diaminopimelic acid (iE-DAP)-triggered BMECs. Butyrate also depressed the protein abundance of myosin light chain kinase (MLCK), elevated the expression of TJ proteins, and restored the cellular distribution of TJ proteins and the barrier function of epithelial cells. HDAC3 overexpression abolished the protective effects of butyrate. In conclusion, butyrate alleviated the iE-DAP-induced inflammatory response and TJ injury by blocking NF-kappa B activation and decreasing inflammatory cytokine production and MLCK expression in a HDAC3-dependent manner. Our finding provides a mechanistic basis for further exploring the regulatory effects of butyrate on the mammary inflammatory response.

Automated summary

The present study demonstrates that butyrate can alleviate the inflammatory response and tight junction (TJ) injury in bovine mammary epithelial cells (BMECs) by blocking NF-kappa B activation and decreasing inflammatory cytokine production and myosin light chain kinase (MLCK) expression.