Pregnancy and spontaneous fetal loss: A pig perspective

Abstract

Pigs have a unique, non-invasive epitheliochorial placenta where maternal and fetal layers lay in apposition. Indentation of fetal capillaries into the trophoblasts and maternal capillaries into the uterine epithelium reduce the distance between the fetal and maternal blood, ensuring nutrient transfer for proper conceptus development. Another unique feature of pig pregnancy is conceptus-mediated immune cell enrichment during the early stages of conceptus attachment (around gestation Day 15). This period coincides with the development of vasculature networks at the maternal-fetal interface, which is critical for successful conceptus growth. Specific chemokines, their receptors, and chemokine decoy receptor networks coordinate this immune cell enrichment and the positioning at the maternal-fetal interface. The recruited immune cells, in turn, adopt a specialized phenotype to support key processes of maternal-fetal adaptations, including tolerance to the semi-allogeneic fetus and supporting vascularization. Disturbance in coordinated cross talk between the conceptus and maternal endometrium is an important mechanism associated with spontaneous fetal loss. The exact mechanism of fetal loss is still not yet identified, although research in the last two decades point to various factors including genetics, nutrition, uterine capacity, placental efficiency, and imbalanced immune factors at the maternal-fetal interface. In this review, we summarize some of the recent advances in endometrial immune cell functions and their regulation. We also provide insights into endometrial/placental transcriptome, microRNA biology, and extravesicular transport across the maternal-fetal interface, as well as their potential implications in porcine pregnancy success or failure.