Both n-3 and n-6 polyunsaturated fatty acids (PUFAs) are derived from the diet, with concentrations in the reproductive tract reflecting dietary intake. PUFAs have multiple functions: as precursors to eicosanoids, regulators of steroid biosynthesis, inflammatory mediators and supplying energy (particularly in oocytes). The PUFA composition of cell membranes affects signalling pathways and susceptibility to oxidative damage. All of these roles may influence reproduction although results are often inconsistent between studies. Supplementation of cows with various PUFAs can increase the numbers of antral follicles although work on polyovular species (pigs, rodents) has usually failed to detect a change in ovulation rate. The anti-inflammatory actions of n-3 PUFAs may reduce follicular PGE production, delaying ovulation and allowing ovulatory follicles to grow larger and produce more steroid. Various PUFA supplements can reduce the interval from calving until first ovulation in cattle although the mechanism is uncertain. Both n-3 and n-6 PUFA supplements have been fed to various species before collecting oocytes for in vitro fertilization. Positive, negative and no effects on subsequent embryo development have all been reported. When PUFAs are added directly to oocyte maturation medium, high doses of linoleic acid (18:2 n-6) are consistently deleterious, while α-linolenic acid (18:3n-3) has been associated with positive outcomes. Uterine prostaglandin production regulates luteal regression and pregnancy recognition. Supplementary n-3 PUFAs have either increased or decreased PGF2α production in different studies. There is some evidence that cattle and pigs fed a PUFA supplement post insemination may have an increased pregnancy rate.

The innate immune response of the endometrium is crucial to achieve early and quick defence against pathogenic organisms that invade the reproductive tract and the uterus, before the adaptive immune response which develops much later. This early innate response is important to avoid the development of uterine disease that impacts negatively on fertility. This review is focused on the regulation of innate immunity within the bovine endometrium during infection. Although a phagocytic barrier to infection is provided by leucocytes, many recent studies have increasingly recognized the important roles of endometrial epithelial and stromal cells in early microbial detection, cellular and inter-cellular signalling, and secretion of immune/inflammatory mediators that can promote leucocyte recruitment and migration to the uterus and endometrium. Components of the endometrial innate immune response involve an increase in the expression of inflammatory products and innate immune mediators including antimicrobial peptides, mucins, pro-inflammatory cytokines including chemokines, acute phase proteins, type I interferons and prostaglandins. However, endometrial innate immunity can be influenced by many factors including infection with a number of pathogenic bacteria, viruses such as bovine viral diarrhoea virus and bovine herpes virus-4; fluctuating levels of the ovarian steroid hormones oestradiol and progesterone; and periparturient changes in body metabolism involving energy substrates and metabolites, metabolic hormones and protein metabolites. This review highlights the recent understandings on how these factors may regulate the endometrial innate immunity, although some of the underlying mechanisms are not yet clearly defined.