Cortisol inhibits lipopolysaccharide-induced inflammatory response in bovine endometrial stromal cells via NF-kB and MAPK signaling pathways

Bovine uterine infection is commonly caused by Escherichia coli (E. coli). Elevated concentrations of plasma cortisol have been reported in postpartum cows. However, the direct role of cortisol in the inflammatory response of bovine endometrial stromal cells (BESCs) remains unclear. Therefore, the aim of the study was to explore the regulatory effect of cortisol on lipopolysaccharide (LPS)-induced inflammatory response in BESCs. Both the primary and immortalized BESCs were used in this study. BESCs were treated with cortisol (5, 15, and 30 ng/mL) in the presence of LPS. The mRNA expression of inflammatory cytokines and chemokines was detected using RT-qPCR. Western blot and immunofluorescence were used to analyze the activation of the NF-.B and MAPK signaling pathways. The results revealed that cortisol downregulated the LPS-induced overexpression of interleukin(IL)-1 ss, IL-6, IL-8, TNF-a, COX-2, iNOS in BESCs. Moreover, cortisol inhibited LPS-induced phosphorylation levels of I.B, p65, ERK1/2, JNK and p38, and p65 nuclear translocation in BESCs. These results indicated that cortisol inhibited LPS-induced inflammatory response in BESCs, which may be mediated by suppressing the NF-.B and MAPK signaling pathways.