Progesterone inhibits inflammatory response in E.coli- or LPS-Stimulated bovine endometrial epithelial cells by NF-κB and MAPK pathways.

Progesterone suppresses the innate immune function of bovine endometrium, making the uterus susceptible to bacterial infection. The bovine endometrial epithelial cells (BEEC) are the first line of defense against bacteria, such as Escherichia coli (E.coli) that causes inflammation of endometrium through the recognition of lipopolysaccharide (LPS). The aim of this study was to investigate the effect of progesterone on the inflammatory response and its potential mechanism using E.coli- or LPS-induced BEEC. Concentrations of 1, 3 and 5 ng/mL progesterone were selected. The mRNA expressions of proinflammatory cytokines were determined using qPCR. The activations of NF-κB and MAPK pathways were detected by Western blot and immunofluorescence. An increase in the mRNA expression of IL-1β, IL-6, IL-8 and TNF-α was observed in BEEC treated with progesterone, LPS or E.coli alone. Progesterone inhibited the E.coli- or LPS-induced gene expression of these cytokines. Progesterone treatment alone showed little influence on NF-κB or MAPK pathway. In BEEC stimulated with E.coli or LPS, progesterone inhibited the phosphorylations of IκB, p65, ERK1/2, p38MAPK and JNK, and the translocation of p65 into the nucleus. These results suggested that progesterone has anti-inflammatory effect, which may be mediated by inhibiting NF-κB activation and MAPK phosphorylation in BEEC.