Infertility is a worldwide problem affecting the cattle industry. Despite most inseminations resulting in successful fertilisation, embryonic and foetal mortality occurs in about 50% of the cases, with an estimated 70–80% of losses sustained before implantation. Due to beef and dairy constituting 20.8% of the EU agricultural output, reproductive inefficiency translates into a tremendous social and bioeconomic impact. Although many factors can be involved in preimplantation loss, there is increasing evidence for the role of the maternal immune system and its regulation by seminal plasma (SP). Studies in rodents, humans and pigs have described beneficial effects of SP in improving embryo development and implantation. However, evidence for a role of SP in fertility in cattle, where removal of SP before artificial insemination is routine, is relatively weak. Thus, this project will use a model of heifers mated to vasectomised (a bull in which the vas deferens has been sectioned, so that the only contribution to the ejaculate comes from the accessory glands, i.e the ejaculate is made of SP with no sperm) or intact bulls (the ejaculate will be comprised of SP and sperm), to study the role of SP in paternal-maternal communication as it pertains to embryo development and immune modulation. If the beneficial effects of SP on fertility is recapitulated in cattle, the associated increased production and efficiency could have a tremendous impact in the beef and dairy industries.
The specific objectives are:
1) To interrogate the global transcriptome profiles of endometrium from heifers mated to vasectomised or intact bulls, and compare it to a cyclic control. Sperm have the potential to transport SP components to distal areas of the reproductive tract, in addition to having a direct effect on these tissues.
2) To characterise the protein composition of uterine fluid after exposure to SP and sperm so that we can evaluate the biological effect of the transcriptomic changes studied in the previous objective. As this is the environment in which the early embryo resides, it will give a notion of paternally-derived changes that drive embryo development.
3) To histologically characterise the immune cell population in the oviduct and uterine horn after exposure to SP and sperm. This will provide information about the recruitment of immune cells to the female reproductive tract by SP or sperm. Together with the results obtained from accomplishing the previous two objectives, it will provide evidence on whether paternal factors play a role in the modulation of the female immune response toward the semi-allogeneic embryo.
4) To assess size and developmental markers in conceptuses recovered from females exposed to SP, and compare them to those collected from control animals. This will determine whether the possible changes that we observe in the female environment translate into an enhanced developmental potential of the early embryo.
