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 ArticleDOI
Pregnancy and preeclampsia affect monocyte subsets in humans and rats.
Barbro N. Melgert,Barbro N. Melgert,Floor Spaans,Theo Borghuis,Pieter Klok,Bart B. L. Groen,Annemarie Bolt,Paul de Vos,Maria G. van Pampus,Tsz Y. Wong,Harry van Goor,Winston W. Bakker,Marijke M. Faas +12 more
TL;DR: The observation that ATP stimulated numbers/activation of nonclassical monocytes in pregnant rats only, suggests that nonclassicals monocytes are specifically altered in pregnancy and may play a role in the pathophysiology of preeclampsia.
Journal ArticleDOI
Administration of Interleukin-17 Soluble Receptor C Suppresses TH17 Cells, Oxidative Stress, and Hypertension in Response to Placental Ischemia During Pregnancy
Denise C. Cornelius,James P. Hogg,Jeremy Scott,Kedra Wallace,Florian Herse,Janae Moseley,Gerd Wallukat,Ralf Dechend,Babbette LaMarca +8 more
TL;DR: It is shown that infusion of IL-17RC blunts TH17s, oxidative stress, AT1-AA, and hypertension in the RUPP model of preeclampsia, indicating that TH17 cells may play an important role in disease pathophysiology.
Journal ArticleDOI
Activation of NF-κB in Placentas of Women with Preeclampsia
John E. Vaughan,Scott W. Walsh +1 more
TL;DR: Oxidative stress causes NF-κB activation in a trophoblast-like cell line, which is enhanced by TNFα, and data suggest that oxidative stress is likely an important in vivo activator of placental NF-σB in preeclampsia.
Journal ArticleDOI
Are Early and Late Preeclampsia Distinct Subclasses of the Disease--What Does the Placenta Reveal?
TL;DR: The contention that early- and late-onset preeclampsia are different subclasses of disease is supported, as clear histopathological differences in placentas showed clear histopathyological differences, whereas late-ONSet preeClampsia and normal term placenta differed less.
Journal ArticleDOI
Cytotrophoblast differentiation in the first trimester of pregnancy: evidence for separate progenitors of extravillous trophoblasts and syncytiotrophoblast
TL;DR: It is speculated that as early as 8 weeks of gestation there are two separate villous cytotrophoblasts populations, one committed to differentiate into syncytiotrophoblast and the second committed to the extravillous differentiation pathway.
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