Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

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

Item Type:Article
Title:Proliferation of endogenous regulatory T cells improve the pathophysiology associated with placental ischaemia of pregnancy
Creators Name:Ibrahim, T. and Przybyl, L. and Harmon, A.C. and Amaral, L.M. and Faulkner, J.L. and Cornelius, D. and Cunningham, M.W. and Hünig, T. and Herse, F. and Wallukat, G. and 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

Repository Staff Only: item control page

Open Access
MDC Library