ST2 and IL-33 in pregnancy and pre-eclampsia

Normal pregnancy is associated with a mild systemic inflammatory response and an immune bias towards type 2 cytokine production, whereas pre-eclampsia is characterized by a more intense inflammatory response, associated with endothelial dysfunction and a type 1 cytokine dominance. Interleukin (IL)-3...

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Published in:PloS one 2011-09, Vol.6 (9), p.e24463-e24463
Main Authors: Granne, Ingrid, Southcombe, Jennifer H, Snider, James V, Tannetta, Dionne S, Child, Tim, Redman, Christopher W G, Sargent, Ian L
Format: Article
Language:English
Subjects:
Adult
Age
Asthma
Bias
Biology
Cytokines
Disease
Endothelium
Explants
Female
Gangrene
Gene Expression Regulation
Gynecology
Heart attacks
Humans
Hypoxia
Inflammation
Inflammatory response
Interleukin 1
Interleukin-1 Receptor-Like 1 Protein
Interleukin-33
Interleukins
Interleukins - blood
Interleukins - metabolism
Ligands
Lysates
Medicine
Mortality
Obstetrics
Perfusion
Placenta
Placenta - metabolism
Placenta - secretion
Pre-eclampsia
Pre-Eclampsia - blood
Preeclampsia
Pregnancy
Pregnant women
Receptors, Cell Surface - blood
Receptors, Cell Surface - chemistry
Receptors, Cell Surface - metabolism
Reperfusion
Sepsis
Solubility
Transcription factors
Tumor necrosis factor-TNF
Vascular endothelial growth factor
Womens health
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cited_by cdi_FETCH-LOGICAL-c691t-38a5bf905277e7508f60514f095fbf53b5fc245ae50aeeef5a0bb5f1eefa12133
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container_issue 9
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container_title PloS one
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creator Granne, Ingrid
Southcombe, Jennifer H
Snider, James V
Tannetta, Dionne S
Child, Tim
Redman, Christopher W G
Sargent, Ian L
description Normal pregnancy is associated with a mild systemic inflammatory response and an immune bias towards type 2 cytokine production, whereas pre-eclampsia is characterized by a more intense inflammatory response, associated with endothelial dysfunction and a type 1 cytokine dominance. Interleukin (IL)-33 is a newly described member of the IL-1 family, which binds its receptor ST2L to induce type 2 cytokines. A soluble variant of ST2 (sST2) acts as a decoy receptor to regulate the activity of IL-33. In this study circulating IL-33 and sST2 were measured in each trimester of normal pregnancy and in women with pre-eclampsia. While IL-33 did not change throughout normal pregnancy, or between non-pregnant, normal pregnant or pre-eclamptic women, sST2 was significantly altered. sST2 was increased in the third trimester of normal pregnancy (p
doi_str_mv 10.1371/journal.pone.0024463
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Interleukin (IL)-33 is a newly described member of the IL-1 family, which binds its receptor ST2L to induce type 2 cytokines. A soluble variant of ST2 (sST2) acts as a decoy receptor to regulate the activity of IL-33. In this study circulating IL-33 and sST2 were measured in each trimester of normal pregnancy and in women with pre-eclampsia. While IL-33 did not change throughout normal pregnancy, or between non-pregnant, normal pregnant or pre-eclamptic women, sST2 was significantly altered. sST2 was increased in the third trimester of normal pregnancy (p&lt;0.001) and was further increased in pre-eclampsia (p&lt;0.001). This increase was seen prior to the onset of disease (p&lt;0.01). Pre-eclampsia is a disease caused by placental derived factors, and we show that IL-33 and ST2 can be detected in lysates from both normal and pre-eclampsia placentas. ST2, but not IL-33, was identified on the syncytiotrophoblast layer, whereas IL-33 was expressed on perivascular tissue. In an in vitro placental perfusion model, sST2 was secreted by the placenta into the 'maternal' eluate, and placental explants treated with pro-inflammatory cytokines or subjected to hypoxia/reperfusion injury release more sST2, suggesting the origin of at least some of the increased amounts of circulating sST2 in pre-eclamptic women is the placenta. 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In an in vitro placental perfusion model, sST2 was secreted by the placenta into the 'maternal' eluate, and placental explants treated with pro-inflammatory cytokines or subjected to hypoxia/reperfusion injury release more sST2, suggesting the origin of at least some of the increased amounts of circulating sST2 in pre-eclamptic women is the placenta. These results suggest that sST2 may play a significant role in pregnancies complicated by pre-eclampsia and increased sST2 could contribute to the type 1 bias seen in this disorder.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21949719</pmid><doi>10.1371/journal.pone.0024463</doi><tpages>e24463</tpages><oa>free_for_read</oa></addata></record>
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1932-6203
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source Publicly Available Content Database; PubMed Central(OpenAccess)
subjects Adult
Age
Asthma
Bias
Biology
Cytokines
Disease
Endothelium
Explants
Female
Gangrene
Gene Expression Regulation
Gynecology
Heart attacks
Humans
Hypoxia
Inflammation
Inflammatory response
Interleukin 1
Interleukin-1 Receptor-Like 1 Protein
Interleukin-33
Interleukins
Interleukins - blood
Interleukins - metabolism
Ligands
Lysates
Medicine
Mortality
Obstetrics
Perfusion
Placenta
Placenta - metabolism
Placenta - secretion
Pre-eclampsia
Pre-Eclampsia - blood
Preeclampsia
Pregnancy
Pregnant women
Receptors, Cell Surface - blood
Receptors, Cell Surface - chemistry
Receptors, Cell Surface - metabolism
Reperfusion
Sepsis
Solubility
Transcription factors
Tumor necrosis factor-TNF
Vascular endothelial growth factor
Womens health
title ST2 and IL-33 in pregnancy and pre-eclampsia
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