Proliferation of endogenous regulatory T cells improve the pathophysiology associated with placental ischaemia of pregnancy
[ 1 ] Instytut Chemii Bioorganicznej Polskiej Akademii Nauk, Polska Akademia Nauk | [ P ] pracownik
2017
artykuł naukowy
angielski
EN ProblemPreeclampsia (PE) is associated with inflammation and decreased Treg cells and IL-10. The reduced uterine perfusion pressure (RUPP) rat model of PE exhibits these characteristics, and we hypothesized that induction of endogenous Tregs by a specific stimulus (CD28 superagonistic monoclonal antibody) would reduce inflammation, vasoactive factors, and hypertension in RUPP rats. Method of studyRUPP was performed at gestation day (GD) 14; CD28 superagonist was administered intraperitoneally GD15; GD18 carotid catheters were inserted, and GD19 MAP and pup weight, blood, and tissues were collected. ResultsMAP (mmHg) in NP rats was 995 and 122 +/- 2 in RUPPs and was 111 +/- 1mmHg in RUPP+SA. Circulating Tregs were 6 +/- 2% in NP rats and 0.77 +/- 0.49% in RUPP rats but increased to 11 +/- 3% in RUPP+SA rats. Circulating IL-6 and IL-2 were decreased while IL-10 and TGF-B were significantly increased in RUPP+SA compared to RUPP controls. Vasoactive pathways such as ET-1, AT1-AA, and ROS were all reduced in RUPP+SA compared to RUPP. Pup weight was 2.4 +/- 0.05mg in NP and 1.94 +/- 0.062mg in RUPP and increased to 2.1 +/- 0.05mg in RUPP+SA. ConclusionThese data suggest that stimulating endogenous Tregs lower factors causing hypertension and can improve fetal weight in response to PE.
e12724
CC BY (uznanie autorstwa)
ostateczna wersja opublikowana
07.2017
przed opublikowaniem
30
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