Influence of semen on inflammatory modulators of embryo implantation

Abstract

Insemination transmits to the female reproductive tract constituents of seminal plasma that target uterine epithelial cells to activate a cascade of inflammatory and immunological changes. Experiments in rodents show seminal factor signalling acts to 'condition' the female immune response to tolerate the conceptus, and to organise molecular and cellular changes in the endometrium to facilitate embryo development and implantation. The active factors in seminal plasma are identified as members of the transforming growth factor-beta family, with the relative balance of active moieties influencing the precise character of the female tract response. Experiments in rodents show that disruption of seminal plasma priming causes foetal growth retardation and changes in placental structure, with long-term consequences for the growth of the neonate. Recent studies indicate a similar physiological function and molecular basis for seminal plasma actions in the pig. In gilts, seminal plasma elicits an endometrial response characterised by recruitment of inflammatory leukocytes and induction of several pro-inflammatory cytokines and cyclo-oxygenase-2. The consequences are evident throughout the pre-implantation period of early pregnancy with altered leukocyte populations and cytokine parameters seen for at least 9 days. Exposure to semen also alters the dynamics in pre-implantation embryo development with an increase in the number of embryos and in their viability. Furthermore seminal plasma influences the temporal kinetics of ovulation, corpus luteum development and steroid production in the ovary. Dissecting the actions of seminal plasma may facilitate development of strategies to ensure maximal fertility and reduce embryo mortality in the pig.