Author:
Cheng Zhangrui,Abudureyimu Ayimuguli,Oguejiofor Chike F,Ellis Rebekah,Barry Amy Teresa,Chen Xing,Anstaett Olivia L,Brownlie Joe,Wathes D Claire
Abstract
AbstractEmbryonic mortality in cows is at least in part caused by failure of pregnancy recognition (PR). Evidence has shown that bovine viral diarrhoea virus (BVDV) infection can disrupt pregnancy. Prostaglandins (PG) play important roles in many reproductive processes, such as implantation. The aim of this study was to investigate the effect of BVDV infection on uterine PG production and PR using anin vitroPR model. Bovine uterine endometrial cells isolated from ten BVDV-free cows were cultured and treated with 0 or 100ng/mL interferon-τ (IFNT) in the absence or presence of non-cytopathic BVDV (ncpBVDV). PGF2αand PGE2concentrations in the spent medium were measured using radioimmunoassays, and in the treated cells expression of the genes associated with PG production and signalling was quantified using qPCR. The results showed that the IFNT challenge significantly stimulatedPTGS1andPTGER3mRNA expression and PGE2production; however, these stimulatory effects were neutralised in the presence of ncpBVDV infection. ncpBVDV infection significantly increasedPTGS1andmPGES1mRNA expression and decreasedAKR1B1expression, leading to increased PGE2and decreased PGF2αconcentrations and an increased PGE2:PGF2αratio. The other tested genes, includingPGR,ESR1,OXTR,PTGS2,PTGER2andPTGFR, were not significantly altered by IFNT, ncpBVDV or their combination. Our study suggests that BVDV infection may impair PR by (1) inhibiting the effect of IFNT on uterine PG production and (2) inducing an endocrine switch of PG production from PGF2αto PGE2to decrease uterine immunity, thereby predisposing the animals to uterine disease.
Subject
Cell Biology,Obstetrics and Gynecology,Endocrinology,Embryology,Reproductive Medicine