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...
| Egile Nagusiak: | , , , , , , |
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| Formatua: | Journal article |
| Hizkuntza: | English |
| Argitaratua: |
2011
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| _version_ | 1826265110874685440 |
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| author | Granne, I Southcombe, J Snider, J Tannetta, D Child, T Redman, C Sargent, I |
| author_facet | Granne, I Southcombe, J Snider, J Tannetta, D Child, T Redman, C Sargent, I |
| author_sort | Granne, I |
| collection | OXFORD |
| 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. |
| first_indexed | 2024-03-06T20:18:33Z |
| format | Journal article |
| id | oxford-uuid:2d001e08-03bf-48fe-acdf-c572a9fb3931 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T20:18:33Z |
| publishDate | 2011 |
| record_format | dspace |
| spelling | oxford-uuid:2d001e08-03bf-48fe-acdf-c572a9fb39312022-03-26T12:40:12ZST2 and IL-33 in pregnancy and pre-eclampsia.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:2d001e08-03bf-48fe-acdf-c572a9fb3931EnglishSymplectic Elements at Oxford2011Granne, ISouthcombe, JSnider, JTannetta, DChild, TRedman, CSargent, INormal 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. |
| spellingShingle | Granne, I Southcombe, J Snider, J Tannetta, D Child, T Redman, C Sargent, I ST2 and IL-33 in pregnancy and pre-eclampsia. |
| title | 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_short | ST2 and IL-33 in pregnancy and pre-eclampsia. |
| title_sort | st2 and il 33 in pregnancy and pre eclampsia |
| work_keys_str_mv | AT grannei st2andil33inpregnancyandpreeclampsia AT southcombej st2andil33inpregnancyandpreeclampsia AT sniderj st2andil33inpregnancyandpreeclampsia AT tannettad st2andil33inpregnancyandpreeclampsia AT childt st2andil33inpregnancyandpreeclampsia AT redmanc st2andil33inpregnancyandpreeclampsia AT sargenti st2andil33inpregnancyandpreeclampsia |