PSII-A-11 Suppressing the Cxcl12-Cxcr4 Chemokine Axis at the Fetal-Maternal Interface During Implantation Results in Altered Expression of Inflammatory Cytokines in Ovine Placenta at Midgestation

Abstract A proper balance of pro and anti-inflammatory cytokines at the fetal-maternal interface is crucial for successful embryo implantation placental formation (placentation) during early gestation. However, mechanisms controlling this inflammatory profile are not well characterized. The C-X-C motif chemokine ligand 12 (CXCL12) its receptor CXCR4 expressed by fetal maternal tissues implicated in cytokine synthesis; roles axis placentation unclear. Using an vivo sheep model, we demonstrated that suppressing CXCL12-CXCR4 signaling results dysregulated production placenta. objective current study was to determine if disrupted from gestation would result altered midgestation. On day post-breeding, osmotic pumps were surgically installed 37 ewes delivered either inhibitor (AMD3100) 1X dose, (n=8), 1.5X, or 3X, (n=8) saline (n=13) into uterine lumen ipsilateral corpus luteum 14 days. days 90 135, collected, placenta components separated analyzed. Gene expression select analyzed using Real-time qPCR. 90, mRNA significantly AMD3100 treatment tumor necrosis factor (TNF), interleukin (IL-12), transforming growth beta (TGFB) Expression TGFB also compared control on 135 whereas IL-12 135. In conclusion, modulating CXCL12-induced actions a novel approach manipulating environment when most pregnancy losses occur. Increasing our understanding will hopefully reveal methods improve reproductive success health livestock.