Abstract
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-κB activation, and thus suppressed inflammatory cytokine production in γ-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-κB 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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
