LncRNA XIST mediates bovine mammary epithelial cell inflammatory response via NF-kappa B/NLRP3 inflammasome pathway

Objectives The correlations between long non-coding RNAs (lncRNAs) and diverse mammal diseases have been clarified by many researches, but the cognition about bovine mastitis-related lncRNAs remains limited. This study aimed to investigate the potential role of lncRNA X-inactive specific transcript (XIST) in the inflammatory response of bovine mammary epithelial cells. Materials and methods Two inflammatory bovine mammary alveolar cell-T (MAC-T) models were established by infecting the cells with Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus). The expressions of pro-inflammatory cytokines were measured, and the proliferation, viability and apoptosis of the inflammatory cells were evaluated after XIST was knocked down by an siRNA. The relationship among XIST, NF-kappa B pathway and NOD-like receptor protein 3 (NLRP3) inflammasome was investigated using an inhibitor of NF-kappa B signal pathway. Results The expression of XIST was abnormally increased in bovine mastitic tissues and inflammatory MAC-T cells. Silencing of XIST significantly increased the expression of E. coli or S. aureus-induced pro-inflammatory cytokines. Additionally, knockdown of XIST could inhibit cell proliferation, suppress cell viability and promote cell apoptosis under inflammatory conditions. Furthermore, XIST inhibited E. coli or S. aureus-induced NF-kappa B phosphorylation and the production of NLRP3 inflammasome. Conclusions The expression of XIST was promoted by activated NF-kappa B pathway and, in turn, XIST generated a negative feedback loop to regulate NF-kappa B/NLRP3 inflammasome pathway for mediating the process of inflammation.