Identifying immune mechanisms mediating the hypertension during preeclampsia.
Preeclampsia (PE) is a pregnancy-associated disorder that affects 5-8% of pregnancies and is a major cause of maternal, fetal, and neonatal morbidity and mortality. Hallmark characteristics of PE are new onset hypertension after 20 wk gestation with or without proteinuria, chronic immune activation, fetal growth restriction, and maternal endothelial dysfunction. However, the pathophysiological mechanisms that lead to the development of PE are poorly understood. Recent data from studies of both clinical and animal models demonstrate an imbalance in the subpopulations of CD4+ T cells and a role for these cells as mediators of inflammation and hypertension during pregnancy. Specifically, it has been proposed that the imbalance between two CD4+ T cell subtypes, regulatory T cells (Tregs) and T-helper 17 cells (Th17s), is involved in the pathophysiology of PE. Studies from our laboratory highlighting how this imbalance contributes to vasoactive factors, endothelial dysfunction, and hypertension during pregnancy will be discussed in this review. Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role.
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, Mississippi bblamarca@umc.edu.
Babbette
B
LaMarca
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Denise C
DC
Cornelius
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Ashlyn C
AC
Harmon
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Lorena M
LM
Amaral
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Mark W
MW
Cunningham
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Jessica L
JL
Faulkner
Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, Mississippi.
Kedra
K
Wallace
D000328:Adult; D005260:Female; D006801:Humans; D046110:Hypertension, Pregnancy-Induced / Q000276:immunology* / Q000503:physiopathology; D011225:Pre-Eclampsia / Q000276:immunology* / Q000503:physiopathology; D011247:Pregnancy; D013601:T-Lymphocytes / Q000276:immunology
cytokines; hypertension; inflammation; pregnancy