Abstract P101: Interleukin 17 Signaling Mediates Cytolytic Natural Killer Cell Activation in Response to Placental Ischemia

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2019-09, Vol.74 (Suppl_1)
• Main Authors: Cornelius, Denise C, Travis, Olivia K, White, Dakota, Baik, Cedar H, Thompson, Willie L, Giachelli, Chelsea, Williams, Jan M, LaMarca, Babbette
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.74.suppl_1.P101

Abstract only The R educed U terine P erfusion P ressure (RUPP) rat model of placental ischemia mimics many characteristics of preeclampsia (PE) including hypertension, fetal growth restriction, and increased T H 17s, IL-17, and cytolytic natural killer cells (cNKs). IL-17 stimulates NK cytotoxicity in vitro . This study tested the hypothesis that blockade of IL-17 signaling would inhibit activation of cNKs to improve blood pressure and fetal growth in RUPP rats. On gestation day (GD) 14, osmotic pumps infusing IL-17 RC (100 pg/d), a soluble receptor for IL-17, were implanted into pregnant rats undergoing RUPP (RUPP+IL17 RC). On GD 19, circulating and placental T H 17s and cNKs were quantified via flow cytometry in normal pregnant (NP), RUPP, and RUPP+IL17 RC rats. cNK activation, placental ROS, fetal and placental weights, and MAP were also assessed. As we have previously shown, placental T H 17 populations (% gated) were significantly increased in RUPP (23.1±3.9%, n=9) compared to NP (8.5±3.9%, n=9) rats and were suppressed in RUPP+IL17 RC (8.3±3.1%, n=9). Circulating T H 17s followed the same trend. Placental cNKs, significantly increased from 7.2±2.8% in NP to 16.6±3.3% in RUPP, and were normalized to 7.2±2.8% after IL-17 blockade (p