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ST2 and IL-33 in pregnancy and pre-eclampsia
Ingrid Granne1, Jennifer H Southcombe, James V Snider
1Oxford Fertility Unit, Nuffield Department of Obstetrics and Gynaecology, University of Oxford, Oxford, United Kingdom.
Plos One
|September 28, 2011
Summary
Soluble ST2 (sST2) levels increase during normal pregnancy and are significantly elevated in pre-eclampsia, even before disease onset. The placenta contributes to this increase, suggesting sST2 plays a role in pre-eclampsia pathogenesis.
Area of Science:
- Immunology
- Reproductive Medicine
- Biochemistry
Background:
- Normal pregnancy involves a mild inflammatory response and a type 2 cytokine bias.
- Pre-eclampsia features a heightened inflammatory response, endothelial dysfunction, and a type 1 cytokine dominance.
- Interleukin-33 (IL-33) and its receptor system, including soluble ST2 (sST2), modulate immune responses.
Purpose of the Study:
- To investigate the levels of IL-33 and sST2 in normal pregnancy and pre-eclampsia.
- To determine the placental contribution to circulating sST2 levels.
- To explore the potential role of sST2 in the immune dysregulation of pre-eclampsia.
Main Methods:
- Measurement of circulating IL-33 and sST2 across trimesters of normal pregnancy and in pre-eclampsia.
- Detection of IL-33 and ST2 in placental tissue.
- Analysis of sST2 secretion from placental explants in an in vitro perfusion model under various conditions.
Main Results:
- Circulating IL-33 levels remained unchanged in normal pregnancy and pre-eclampsia.
- Soluble ST2 (sST2) levels increased in the third trimester of normal pregnancy and were further elevated in pre-eclampsia, preceding disease onset.
- The placenta expresses ST2, and placental explants release sST2, with increased secretion under pro-inflammatory or hypoxia/reperfusion conditions.
Conclusions:
- Elevated sST2, originating partly from the placenta, is a hallmark of pre-eclampsia.
- Increased sST2 may contribute to the type 1 cytokine bias observed in pre-eclampsia.
- The IL-33/sST2 axis is implicated in the pathophysiology of pre-eclampsia.
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