Placentitis is the leading cause of infectious abortion in the horse. Additionally, it can result in weak and/or growth restricted offspring. While the etiology of ascending placentitis is well described in mares, less is known regarding the pathogenesis of other types, such as nocardioform placentitis. This study aims to identify the microbial communities in different body sites of the pregnant mare in early gestation to establish a core microbiome that may be perturbed in pathologic pregnancies such as placentitis. We hypothesize that the equine placenta harbors a distinct resident microbiome in early pregnancy when characterized by metagenetics and that there will be a disparity in bacterial communities from the oral, vaginal, and fecal microbiome. Samples were collected from the oral cavity, vagina, anus, and the allantoic portion of the allantochorion (“placenta”) from five pregnant mares between 96 and 120 days of gestation. The V4 region of the 16S rRNA gene was amplified for Illumina MiSeq sequencing to examine core bacterial communities present in the different body sites. Microbial community composition of the pregnant ponies by body site was significantly different (Bray–Curtis dissimilarity). The placenta was significantly different from the feces, oral cavity, and vagina. Alpha diversity measuring the Shannon diversity matrix was significant, with the body sites being a compounding variable, meaning there was a difference in richness and evenness in the different microbial communities. Feces had the greatest alpha diversity, while the oral cavity and placenta similarly had the least. In conclusion, metagenetics did reveal distinct community differences in the oral, fecal, vaginal, and placenta cavities of the horse. The equine placenta does show similarities in its microbial communities to the oral cavity. Further research needs to be completed to investigate how bacteria may be translocated to the placenta from these other body sites and how they contribute to the development of placentitis.

Insufficient invasion of conceptus-derived trophoblast cells in the maternal decidua is a key event in the development of early-onset preeclampsia (PE), a subtype of PE associated with high maternal and fetal morbidity and mortality. Kisspeptins, a family of peptides previously shown to inhibit trophoblast cell invasion, have been implicated in the pathogenesis of early-onset PE. However, a role of kisspeptin signaling during the genesis of this syndrome has not been elucidated. Herein, we used the preeclamptic-like BPH/5 mouse model to investigate kisspeptin expression and potential upstream regulatory mechanisms in a PE-like syndrome. Expression of the kisspeptin encoding gene, Kiss1, and the 10-amino-acid kisspeptide (Kp-10), are upregulated in the non-pregnant uterus of BPH/5 females during diestrus and in the maternal-fetal interface during embryonic implantation and decidualization. Correspondingly, the dysregulation of molecular pathways downstream to kisspeptins also occurs in this mouse model. BPH/5 females have abnormal sex steroid hormone profiles during early gestation. In this study, the normalization of circulating concentrations of 17β-estradiol (E2) and progesterone (P4) in pregnant BPH/5 females not only mitigated Kiss1 upregulation, but also rescued the expression of multiple molecules downstream to kisspeptin and ameliorated adverse fetoplacental outcomes. Those findings suggest that uterine Kiss1 upregulation occurs pre-pregnancy and persists during early gestation in a PE-like mouse model. Moreover, this study highlights the role of sex steroid hormones in uteroplacental Kiss1 dysregulation and the improvement of placentation by normalization of E2, P4 and Kiss1.