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
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Journal ArticleDOI
Vitamin D and Inflammatory Cytokines in Healthy and Preeclamptic Pregnancies
TL;DR: Maternal and placental calcitriol levels are low in preeclampsia which may explain, at least in part, high pro-inflammatory cytokine levels in this disease.
Journal ArticleDOI
Epigenetic regulation of placental gene expression in transcriptional subtypes of preeclampsia.
Katherine Leavey,Samantha L. Wilson,Shannon Bainbridge,Shannon Bainbridge,Wendy P. Robinson,Brian J. Cox +5 more
TL;DR: DNA methylation alterations underlying a portion of the transcriptional development of “canonical” PE in cluster 2 and “immunological”PE in cluster 3 are established, however, a significant number of the observed methylation changes were not associated with corresponding changes in gene expression, indicating that alternate methods of gene regulation will need to be explored.
Journal ArticleDOI
Are neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), and/or mean platelet volume (MPV) clinically useful as predictive parameters for preeclampsia?
Dominique Mannaerts,Suzanne Heyvaert,Chania De Cordt,Claartje Macken,Charlotte Loos,Yves Jacquemyn +5 more
TL;DR: MPV is significantly elevated in the first half of pregnancy in women who later develop PE and might therefore be implemented in combination with other parameters in a PE prediction model.
Journal ArticleDOI
Maternal Vitamin D Status in the Late Second Trimester and the Risk of Severe Preeclampsia in Southeastern China.
TL;DR: Maternal vitamin D deficiency at 23–28 weeks of gestation was strongly associated with increased odds for severe preeclampsia after adjusting for relevant confounders (adjusted OR, 3.16; 95% CI, 1.77–5.65).
Journal ArticleDOI
Early Disturbed Placental Ischemia and Hypoxia Creates Immune Alteration and Vascular Disorder Causing Preeclampsia
TL;DR: The pathophysiological process that underlies PE has been proposed to occur in two episodes, the first is a reduced placental perfusion and then the maternal clinical syndrome, resulting in a vicious cycle existing within the maternal vasculature as well as within the placental unit.
References
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Journal ArticleDOI
Immunobiology of Dendritic Cells
Jacques Banchereau,Francine Brière,Christophe Caux,Jean Davoust,Serge Lebecque,Yong-Jun Liu,Bali Pulendran,Karolina Palucka +7 more
TL;DR: Dendritic cells are antigen-presenting cells with a unique ability to induce primary immune responses and may be important for the induction of immunological tolerance, as well as for the regulation of the type of T cell-mediated immune response.
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Journal ArticleDOI
Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia
Sharon Maynard,Jiang Yong Min,Jaime R. Merchan,Kee-Hak Lim,Jianyi Li,Susanta Mondal,Towia A. Libermann,James P. Morgan,Frank W. Sellke,Isaac E. Stillman,Franklin H. Epstein,Vikas P. Sukhatme,S. Ananth Karumanchi +12 more
TL;DR: It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia.
Journal ArticleDOI
NF-kappaB regulation in the immune system.
Qiutang Li,Inder M. Verma +1 more
TL;DR: The role of NF-κB proteins as potential therapeutic targets in clinical applications and their role in the immune system and inflammatory diseases are discussed.
Journal ArticleDOI
Circulating Angiogenic Factors and the Risk of Preeclampsia
Richard J. Levine,Sharon Maynard,Cong Qian,Kee-Hak Lim,Lucinda England,Kai F. Yu,Enrique F. Schisterman,Ravi Thadhani,Benjamin P. Sachs,Franklin H. Epstein,Bahaeddine M Sibai,Vikas P. Sukhatme,S. Ananth Karumanchi +12 more
TL;DR: Alterations in the levels of sFlt-1 and free PlGF were greater in women with an earlier onset of preeclampsia and in women in whom preeClampsia was associated with a small-for-gestational-age infant.
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