Reduced uterine perfusion pressure T-helper 17 cells cause pathophysiology associated with preeclampsia during pregnancy

• DOI: 10.1152/ajpregu.00117.2016
• Publication Date: 2016-10-26T23:19:32Z
• Authors: Denise C. Cornelius; Lorena M. Amaral; Kedra Wallace; Nathan Campbell; Alexia J. Thomas; Jeremy Scott; Florian Herse; Gerd Wallukat; Ralf Dechend; Babbette LaMarca
• Keywords: Pathophysiology

Preeclampsia is associated with chronic inflammation and an imbalance among T-helper cell subtypes increase in 17 (TH17) cells. The objective of this study was to determine a role for TH17s, from the reduced uterine perfusion pressure (RUPP) rat model preeclampsia, etiology hypertension during pregnancy. CD4+/CD25- T cells were isolated spleens, cultured TH17 media, verified as TH17s via flow cytometry. On day 12 gestation, 1×106 RUPP rats adoptively transferred into NP rats, carotid catheters inserted on 18, 19, mean arterial (MAP) recorded, serum plasma collected, oxidative stress production agonistic autoantibodies ANG II type I receptor (AT1-AA) analyzed. MAP increased 100.3 ± 1.7 mmHg normal pregnant (NP; n = 17) 124.8 2.1 (n 22; P < 0.0001) 110.8 2.8 NP+RUPP 11). Pup weights decreased 1.92 0.09 g 2.39 0.14 (P 0.01). AT1-AA significantly 0.1 0.2 beats/min 15.6 0.7 TH17s. IL-6 22.3 5.7 pg/ml 60.45 13.8 0.05) 75.9 6.8 Placental renal 238 27.5 411 129.9 relative light units·min-1·mg-1 339 104.6 833 331.1 TH17, respectively. In conclusion, induced intrauterine growth restriction blood pressure, AT1-AA, IL-6, tissue when indicating autoimmune cells, cause much pathophysiology preeclampsia.