Proliferation of endogenous regulatory T cells improve the pathophysiology associated with placental ischaemia of pregnancy

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Item Type:	Article
Title:	Proliferation of endogenous regulatory T cells improve the pathophysiology associated with placental ischaemia of pregnancy
Creators Name:	Ibrahim, T., Przybyl, L., Harmon, A.C., Amaral, L.M., Faulkner, J.L., Cornelius, D., Cunningham, M.W., Hünig, T., Herse, F., Wallukat, G., Dechend, R. and LaMarca, B.
Abstract:	PROBLEM: Preeclampsia (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 STUDY: RUPP 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. RESULTS: MAP (mmHg) in NP rats was 99+/-5 and 122±2 in RUPPs and was 111+/-1 mmHg 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±0.05 mg in NP and 1.94+/-0.062 mg in RUPP and increased to 2.1+/-0.05 mg in RUPP+SA. CONCLUSION: These data suggest that stimulating endogenous Tregs lower factors causing hypertension and can improve fetal weight in response to PE.
Keywords:	Inflammation, Preeclampsia, Regulatory T Cells, Animals, Rats
Source:	American Journal of Reproductive Immunology
ISSN:	1046-7408
Publisher:	Wiley-Blackwell
Volume:	78
Number:	5
Page Range:	e12724
Date:	November 2017
Official Publication:	https://doi.org/10.1111/aji.12724
External Fulltext:	View full text on PubMed Central
PubMed:	View item in PubMed

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