Journal ArticleDOI
A leading role for the immune system in the pathophysiology of preeclampsia
TLDR
The pathophysiology of preeclampsia may involve several factors, including persistent hypoxia at the placental level and the release of high amounts of STBMs, which may contribute to the inflammatory process and to changes in adaptive‐immune system cells, which are also modulated in preeclamping.Abstract:
Preeclampsia syndrome is characterized by inadequate placentation, because of deficient trophoblastic invasion of the uterine spiral arteries, leading to placental hypoxia, secretion of proinflammatory cytokines, the release of angiogenic and antiangiogenic factors and miRNAs. Although immune-system alterations are associated with the origin of preeclampsia, other factors, including proinflammatory cytokines, neutrophil activation, and endothelial dysfunction, are also related to the pathophysiology of this syndrome. The pathophysiology of preeclampsia may involve several factors, including persistent hypoxia at the placental level and the release of high amounts of STBMs. DAMP molecules released under hypoxic conditions and STBMs, which bind TLRs, may activate monocytes, DCs, NK cells, and neutrophils, promoting persistent inflammatory conditions in this syndrome. The development of hypertension in preeclamptic women is also associated with endothelial dysfunction, which may be mediated by various mechanisms, including neutrophil activation and NET formation. Furthermore, preeclamptic women have higher levels of nonclassic and intermediate monocytes and lower levels of lymphoid BDCA-2(+) DCs. The cytokines secreted by these cells may contribute to the inflammatory process and to changes in adaptive-immune system cells, which are also modulated in preeclampsia. The changes in T cell subsets that may be seen in preeclampsia include low Treg activity, a shift toward Th1 responses, and the presence of Th17 lymphocytes. B cells can participate in the pathophysiology of preeclampsia by producing autoantibodies against adrenoreceptors and autoantibodies that bind the AT1-R.read more
Citations
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Journal ArticleDOI
Pre-eclampsia: its pathogenesis and pathophysiolgy.
Prem Gathiram,Jack Moodley +1 more
TL;DR: The central hypothesis is that pre-eclampsia results from defective spiral artery remodelling, leading to cellular ischaemia in the placenta, which in turn results in an imbalance between anti-angiogenic and pro-angIogenic factors.
Journal ArticleDOI
Sterile inflammation and pregnancy complications: a review.
Mathieu Nadeau-Vallée,Dima Obari,Julia Palacios,Marie-Eve Brien,Cyntia Duval,Sylvain Chemtob,Sylvie Girard +6 more
TL;DR: The role of sterile inflammation in reproduction, including early implantation and pregnancy complications is discussed, and major alarmins vastly implicated in numerous sterile inflammatory processes, such as uric acid, HMGB1, IL-1α and cell-free DNA are focused on while giving an overview of the potential role of other candidate alarmins.
Journal ArticleDOI
Nitric Oxide and Reactive Oxygen Species in the Pathogenesis of Preeclampsia
TL;DR: New insights are provided about roles of oxidative stress in the pathophysiology of PE and placental ischemia in PE decreases the antioxidant activity resulting in further elevated oxidative stress, which leads to the appearance of the pathological conditions of PE including hypertension and proteinuria.
Journal ArticleDOI
VEGF may contribute to macrophage recruitment and M2 polarization in the decidua
Karen Wheeler,Manoj Kumar Jena,Manoj Kumar Jena,Bhola S. Pradhan,Neha Nayak,Subhendu Das,Chaur-Dong Hsu,David S. Wheeler,Kang Chen,Nihar R. Nayak +9 more
TL;DR: Dramatic increases in both VEGF levels and macrophage numbers in the decidua during early pregnancy compared to the secretory phase endometrium (non-pregnant), with a significant increase in M2macrophage markers, suggesting that M2 is the predominant macrophages phenotype in thedecidua.
Journal ArticleDOI
Preeclampsia: long-term consequences for vascular health
TL;DR: There is no “cure” for PE except for early delivery of the baby and placenta, leaving PE a health care risk for babies born from PE moms and a risk factor for long-term health in women.
References
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Journal Article
Systemic inflammatory priming in normal pregnancy and preeclampsia: The role of circulating syncytiotrophoblast microparticles (Journal of Immunology (2007) 178, (5949-5956))
Journal ArticleDOI
Hypertension in Response to Placental Ischemia During Pregnancy: Role of B Lymphocytes
Babbette LaMarca,Kedra Wallace,Florian Herse,Gerd Wallukat,James N. Martin,Abram Weimer,Ralf Dechend +6 more
TL;DR: The data demonstrate the important roles that B-lymphocyte activation and agonistic autoantibodies to the angiotensin II type I receptors play in the pathophysiology of hypertension in response to placental ischemia.
Journal ArticleDOI
CD19+CD5+ Cells as Indicators of Preeclampsia
Federico Jensen,Gerd Wallukat,Florian Herse,Oliver Budner,Tarek El-Mousleh,Serban-Dan Costa,Ralf Dechend,Ana Claudia Zenclussen +7 more
TL;DR: A B-cell population able to produce pregnancy-pathological autoantibodies as possible markers for preeclampsia is identified, which opens vast diagnostic and therapeutic applications.
Journal ArticleDOI
Decreased number of FoxP3 + regulatory T cells in preeclampsia
Gergely Toldi,Peter Svec,Barna Vásárhelyi,Gergo Mészáros,János Rigó,Tivadar Tulassay,Tivadar Tulassay,András Treszl +7 more
TL;DR: The proportion of Tregs and that of naive CD4+CD45RA+ cells was lower in preeclamptic women than in control women, which may support the notion that PE shares similar features to autoimmune disorders.
Journal ArticleDOI
A Physiological Function of Inflammation-Associated SerpinB2 Is Regulation of Adaptive Immunity
Wayne A. Schroder,Thuy T. Le,Lee Major,Shayna E. A. Street,Joy Gardner,Eleanore Lambley,Katrina Jane Ivy Markey,Kelli P. A. MacDonald,Richard J. Fish,Ranjeny Thomas,Andreas Suhrbier +10 more
TL;DR: Regulation of Th1 responses appears to be a physiological function of inflammation-associated SerpinB2; an observation that may shed light on human inflammatory diseases like pre-eclampsia, lupus, asthma, scleroderma, and periodontitis.
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