Summary
This project investigates the role of 17-OHPC and PIBF in treating preeclampsia by reducing inflammation and improving pregnancy outcomes, utilizing both a clinical trial and an adoptive transfer rat model.
Project IV
US · IL
NIH
grant
awarded
#nih-1U54HL170290-01A1
What they want
Preeclampsia (PE) is a leading cause of maternal death and perinatal morbidity, characterized by increased CD4+THelper 1 cells, cytokines, autoantibodies (AT1-AA), hypertension, endothelial dysfunction, and intrauterine growth restriction (IUGR), along with decreased progesterone and PIBF. The project hypothesizes that decreased Progesterone/PIBF leads to an inflammatory cascade causing PE symptoms. The research will utilize a clinical trial to test 17-OHPC administration in PE patients and an adoptive transfer rat model of PE using placental CD4+ T cells from PE women, with and without 17-OHPC treatment, and PIBF blockade.
Deliverables
- Data from a clinical trial testing 17-OHPC administration to PE patients, measuring its impact on γδ T cells, PIBF, inflammation, UARI, AT1-AA, sFlt-1, ET-1, HTN, IUGR, and time to delivery.
- Results from an animal model demonstrating whether CD4+ T cells from 17-OHPC-treated PE women cause a PE phenotype in pregnant nude athymic recipient rats.
- Results from an animal model demonstrating whether PIBF blockade in recipient rats of CD4+ T cells from 17-OHPC-treated PE women causes a PE phenotype.
