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The systemic inflammatory response i...
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Borzychowski, Angela Marie.
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The systemic inflammatory response in human pregnancy.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
The systemic inflammatory response in human pregnancy./
作者:
Borzychowski, Angela Marie.
面頁冊數:
214 p.
附註:
Source: Dissertation Abstracts International, Volume: 67-09, Section: B, page: 4992.
Contained By:
Dissertation Abstracts International67-09B.
標題:
Health Sciences, Obstetrics and Gynecology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR17758
ISBN:
9780494177587
The systemic inflammatory response in human pregnancy.
Borzychowski, Angela Marie.
The systemic inflammatory response in human pregnancy.
- 214 p.
Source: Dissertation Abstracts International, Volume: 67-09, Section: B, page: 4992.
Thesis (Ph.D.)--University of Guelph (Canada), 2006.
Successful pregnancy is biased towards humoral (Th2) immune responses, while pathological pregnancies, including pre-eclampsia, are characterized by cell-mediated (Th1) immune responses. The Th1/Th2 paradigm is however, too simplistic since normal pregnancy is characterized by innate immune activation causing a systemic inflammatory response. This is exaggerated in pre-eclampsia. There were two main aims of this thesis. The first was to investigate a role for lymphocytes of the innate immune system in the type 1/type 2 changes during healthy pregnancy and pre-eclamptia. The second was to investigate a role for syncytiotrophoblast microparticles (STBMs), shed from the placenta into the maternal circulation, in the systemic inflammatory response of pregnancy.
ISBN: 9780494177587Subjects--Topical Terms:
1020690
Health Sciences, Obstetrics and Gynecology.
The systemic inflammatory response in human pregnancy.
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Source: Dissertation Abstracts International, Volume: 67-09, Section: B, page: 4992.
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Thesis (Ph.D.)--University of Guelph (Canada), 2006.
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Successful pregnancy is biased towards humoral (Th2) immune responses, while pathological pregnancies, including pre-eclampsia, are characterized by cell-mediated (Th1) immune responses. The Th1/Th2 paradigm is however, too simplistic since normal pregnancy is characterized by innate immune activation causing a systemic inflammatory response. This is exaggerated in pre-eclampsia. There were two main aims of this thesis. The first was to investigate a role for lymphocytes of the innate immune system in the type 1/type 2 changes during healthy pregnancy and pre-eclamptia. The second was to investigate a role for syncytiotrophoblast microparticles (STBMs), shed from the placenta into the maternal circulation, in the systemic inflammatory response of pregnancy.
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In Chapter 1, evidence is presented demonstrating a role for NK and NK-like T cells in the type 2 immune bias of healthy pregnancy, which was evident from twelve weeks of gestation in CD56bright NK cells. Changes in CD56dim NK, NK-like T and Th cells were only apparent during third trimester pregnancy, relative to non-pregnant and pre-eclamptic women, who were characterized by a type 1 immune bias.
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It is unclear what triggers immune changes during pregnancy. However, STBMs may cause leukocyte activation and pro-inflammatory cytokine production, which in turn alter lymphocyte immune responses. In Chapter 2, circulating dendritic cells are shown to bind to STBMs in the periphery during pregnancy. Although the mechanisms of this interaction are not known, changes in the expression of toll-like receptors 2, 4 and 9 and CD14 suggest they may play a role.
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In Chapter 3, an in vitro model is presented for investigating STBM-induced leukocyte activation that was assessed through pro-inflammatory cytokine production. Following STBM stimulation, production of IL-8, IL-12 and TNF-alpha was found by leukocytes from non-pregnant women.
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The results presented in this thesis support innate immune activation during the systemic inflammatory response of pregnancy. It is hypothesized that circulating maternal leukocytes, particularly dendritic cells, are activated by STBMs through CD14 and TLRs, causing pro-inflammatory cytokine production and the systemic inflammatory response. In pre-eclampsia, where this response is excessive, the result is an overall shift to a type 1 immune bias in both T and NK cells.
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