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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Public Library of Science
2011
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3174956/ |
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pubmed-31749562011-09-26 ST2 and IL-33 in Pregnancy and Pre-Eclampsia Granne, Ingrid Southcombe, Jennifer H. Snider, James V. Tannetta, Dionne S. Child, Tim Redman, Christopher W. G. Sargent, Ian L. Research Article 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<0.001) and was further increased in pre-eclampsia (p<0.001). This increase was seen prior to the onset of disease (p<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. 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. Public Library of Science 2011-09-16 /pmc/articles/PMC3174956/ /pubmed/21949719 http://dx.doi.org/10.1371/journal.pone.0024463 Text en Granne et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Granne, Ingrid Southcombe, Jennifer H. Snider, James V. Tannetta, Dionne S. Child, Tim Redman, Christopher W. G. Sargent, Ian L. |
| spellingShingle |
Granne, Ingrid Southcombe, Jennifer H. Snider, James V. Tannetta, Dionne S. Child, Tim Redman, Christopher W. G. Sargent, Ian L. ST2 and IL-33 in Pregnancy and Pre-Eclampsia |
| author_facet |
Granne, Ingrid Southcombe, Jennifer H. Snider, James V. Tannetta, Dionne S. Child, Tim Redman, Christopher W. G. Sargent, Ian L. |
| author_sort |
Granne, Ingrid |
| title |
ST2 and IL-33 in Pregnancy and Pre-Eclampsia |
| title_short |
ST2 and IL-33 in Pregnancy and Pre-Eclampsia |
| title_full |
ST2 and IL-33 in Pregnancy and Pre-Eclampsia |
| title_fullStr |
ST2 and IL-33 in Pregnancy and Pre-Eclampsia |
| title_full_unstemmed |
ST2 and IL-33 in Pregnancy and Pre-Eclampsia |
| title_sort |
st2 and il-33 in pregnancy and pre-eclampsia |
| 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<0.001) and was further increased in pre-eclampsia (p<0.001). This increase was seen prior to the onset of disease (p<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. 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. |
| publisher |
Public Library of Science |
| publishDate |
2011 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3174956/ |
| _version_ |
1611476043054448640 |