Abstract

The aim of the study is to explore the role of Toll-like receptor 4 (TLR4) and immunomodulatory hormones in bovine endometritis. The bovine endometrial epithelial cell model (BenEpC) was used in the study. After contamination by Escherichia coli, BenEpCs were randomly divided into several groups according to the different concentration of 17-β estradiol (E2) treatment and the different stimulation, lipopolysaccharide (LPS) or lipoteichoic acid (LTA). The expressions of TLR4 and COX-2 mRNA were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Prostaglandin F (PGF) and prostaglandin E (PGE) levels were evaluated by radioimmunoassay. A significant difference was observed in TLR4 mRNA expression of bacterial contaminated BEnEpCs among low, middle and high-dose E2 treatment group (p < 0.05). Meanwhile, there was also a statistical difference in the relative changes of theprostaglandin E₂ (PGE₂) and COX-2 mRNA expression in BEnEpCs among low, middle and high-dose E2 treatment group (p < 0.05). Furthermore, the most significant increase of PGE₂and Cyclooxygenase-2 (COX-2) mRNA expression was achieved in the LPS-stimulated BEnEpCs compared with those stimulated with LTA. Our findings suggested that TLR4 was activated in bovine endometritis, and then led to more prostaglandin production as regulation of local inflammatory response. However, this response was dependent on and influenced by the immunomodulatory hormones.

Key words: Bovine endometritis, lipopolysaccharide, toll-like receptor 4, 17-β estradiol.