# Placental Molecular Expression of Different Pathogenic Vaginal Infections

## TL;DR

This study examines how different vaginal infections affect placental markers, which could help predict and prevent pregnancy complications.

## Contribution

The study identifies pathogen-specific changes in placental marker expression, offering new insights into infection-related pregnancy risks.

## Key findings

- GBS and Ureaplasma urealyticum infections show high expression of VDR, CD44, and OPN in placental tissues.
- Klebsiella and Candida infections exhibit lower expression of these markers compared to healthy controls.
- Gram-negative bacteria like Klebsiella show negative IHC staining, indicating immune evasion.

## Abstract

This study evaluated the differential expression of four placental markers—vitamin D receptor (VDR), Cluster of Differentiation 44 (CD44), osteopontin (OPN), and cyclooxygenase-2 (COX-2)—in response to pathogens, which may contribute to our understanding of pathogen-specific impacts on pregnancy outcomes. We immunohistochemically (IHC) analyzed placental tissues obtained from 70 healthy-term pregnant women in the control group and compared them to tissues obtained from 78 women with pregnancy above 24 weeks of gestation, single-pathogen vaginal infection, and premature rupture of membranes/preterm premature rupture of membranes (PROM/PPROM). We detected high expression of these four molecules in cases of Group B Streptococcus (GBS) and Ureaplasma urealyticum vaginal infections, and moderate expression in cases of Enterobacteriaceae infections, except for Klebsiella; the cases with Klebsiella and Candida species (spp.) vaginitis exhibited a lower expression compared to the healthy control group. VDR, CD44, and OPN had increased placental expression in GBS and Ureaplasma urealyticum vaginal infections; the opportunistic pathogenicity of both Escherichia coli and Candida spp. explains their low IHC positivity, and the tremendous ability of Gram-negative bacteria to elude the host immunity is revealed by the negative IHC staining in cases of Klebsiella vaginitis. These findings suggest that pathogen-specific alterations in the expression of these markers may contribute to the differential risk stratification of pregnancy complications and may mitigate the risks of adverse maternal and fetal outcomes. Interventions aiming to modulate these pathways might improve pregnancy outcomes.