Uterine cervix as a fundamental part of the pathogenesis of pregnancy loss associated with ascending placentitis in mares.

This research explores how the uterus in mares responds to pregnancy loss due to an ascending infection, known as placentitis. By inducing placentitis in pregnant mares and studying the molecular and anatomical changes, the study finds that the uterus plays a significant role in the progression of placentitis.

Objective of the Study

• The key objective of this research was to elucidate morphological and molecular changes in the cervix during placentitis in pregnant mares. This was accomplished by analyzing full thickness histology and mRNA expression of various inflammatory and endocrine factors in the cervical mucosa and stroma of the mares.

Methodology

• The researchers used a sample size of five pregnant mares where placentitis was experimentally induced via transcervical inoculation with Streptococcus equi ssp at roughly 290 days of gestation. Four gestational age-matched mares were used as controls.
• They targeted specific gene transcripts related to cervical inflammation including steroid receptors, prostaglandin synthases and receptors, cytokines, and acute phase proteins to document any variations in their transcription.

Key Findings

• The researchers found significant changes in the cervical epithelia and stroma, indicative of cervicitis, a potentially severe condition of the cervix.
• mRNA expression for genes linked to inflammation (IL1β, IL6, CXCL8, SAA) and prostaglandin synthesis (PTGS2) was significantly higher in both the mucosa and stroma of inoculated mares, suggesting an active immune response.
• An upregulation of genes (TNFα, IL10, PGES) was also observed, but only in the cervical mucosa.
• Receptors associated with cervical relaxation in other species, namely, progesterone receptor, ESR1 and PTGER4, were upregulated in the cervical stroma of mares with placentitis.

Conclusion

• The results suggest that the cervix plays a more active role in defending against placentitis, as evidenced by the upregulation of inflammatory cytokines and other factors. This goes beyond its understood role as a physical barrier to the ascending infection.