Inflammatory and Immune System Markers

McKelvey, Kelly; Ariyakumar, Gaayathri; McCracken, Sharon A.

doi:10.1007/978-1-4939-7498-6_7

Cited by 3 publications

(2 citation statements)

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“…When the fetus possesses HLA-C, mothers who lack activating KIR have been shown to have an increased risk of developing preeclampsia. In other words, the reduced expression of HLA-G and HLA-C genes may possibly lead to the suppression of the immune escape from uNK attack (82). These findings strengthen the role of HLA function in the initial step to preeclampsia.…”

Section: Conclusion and Considerationsmentioning

confidence: 52%

Immune‑related pathophysiological causes relevant to a subset of patients with preeclampsia (Review)

et al. 2019

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Preeclampsia is characterized by inadequate extravillous trophoblast (EVT) invasion, leading to feto-placental hypoxia, a release of an excessof anti-angiogenic factors, and finally eliciting maternal endothelial dysfunction and maternal symptoms, such as new-onset hypertension and proteinuria. Despite intensive research over the past decade, the initial pathogenesis of this disorder remains elusive. There are likely different subtypes of preeclampsia and maternal, fetal and placental factors all play an important role in the disease development. In this review, we focus on an immune-related pathway or pathophysiological causes relevant to a subset of patients with preeclampsia. Using the PubMed database, we conducted a literature review of various studies related to the pathogenesis of preeclampsia. The two-stage theory is a notable postulate of the disease. The antecedents of poor placentation are immunological, epigenetic and environmental factors in origin. The causes of inadequate immune mechanisms at the maternal-fetal interface in preeclampsia is considered to be a lack of human leucocyte antigen (HLA) class I molecules, such as HLA-G and HLA-C. A reduction in HLA molecules facilitate EVTs to elicit an immune attack that furthers cell killing. A series of the HLA-G promoter region on EVTs has been found to be more highly methylated in preeclampsia than in normal pregnancy, possibly due to the increased expression of DNA methyltransferase-1 (DNMT-1). Promoter hypermethylation is one of the major epigenetic alterations that may prime for HLA-G gene inactivation. Epigenetic alterations are reversible, and nutrition, lifestyle and environmental factors may be the epigenetic regulators that modify gene expression. However, the timing, cause and underlying mechanisms of HLA gene methylation have not yet been fully established. The adverse intrauterine environment that contributes to immune responses, inflammation, or oxidative stress may be associated with increased susceptibilities for a number of adult diseases, including preeclampsia. We have hypothesized that close interactions between the inherited epigenetic architecture (hypermethylation of HLA molecules) and adverse intrauterine environmental exposures (oxidative stress and inflammation) leading to epigenetic modifications and to the aberrant DNA methylation of HLA class I molecules, may act as an early event of preeclampsia development.

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Section: Conclusion and Considerationsmentioning

confidence: 52%

Immune‑related pathophysiological causes relevant to a subset of patients with preeclampsia (Review)

et al. 2019

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“…It is characterized by vascular dysfunction and exacerbated inflammation [2][3][4][5][6]. This disorder is often associated with changes in the levels of cytokines, chemokines, blood coagulation factors, and apoptotic markers [7]. In most cases, PE leads to multi-organ failure in the mother such as renal insufficiency, liver dysfunction, neurological or hematological complications, uteroplacental dysfunction and is responsible for significant maternal and perinatal morbidity and mortality.…”

Section: Introductionmentioning

confidence: 99%

Low Serum-Derived Syncytin-2 Levels in Exosome at Early Pregnancy is a Predictor of Preeclampsia: A Prospective Pilot Study in Benin, West Africa

Lokossou¹

2020

J Obst Gynecol Surg

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Preeclampsia (PE) affects 2 to 8% of pregnant women and represents one of the major causes of maternal and perinatal morbidity and mortality, particularly in sub-Saharan Africa. A limited number of biomarkers have been proposed for the identification of pregnant women predisposed to preeclampsia. Syncytin-2 is an endogenous retrovirus envelope protein playing a key role in placental formation through the fusion of villous cytotrophoblasts, resulting in syncytiotrophoblast formation. The reduction of Syncytin-2 levels detected in placental tissue and on the surface of exosomes has been shown to strongly correlate with the severity of symptoms in preeclamptic patients. We were thus interested in conducting an analysis of a Benin cohort of pregnant women over the predictive value of this marker. From July 2015 to January 2017, 260 pregnant women were recruited in two health facilities. Blood samples were monthly collected from the beginning of pregnancy up to 20 weeks of gestation and exosomes were then isolated. We then compared Syncytin-2 levels in exosome preparations from women who presented PE to those with normal pregnancy. Our results showed that Syncytin-2 significantly decreased between 7 to 10 weeks of gestation in pregnant women with PE compared to normal pregnant women (p=0.02). Our study thereby suggests that Syncytin-2 could be a promising biomarker for early diagnosis of PE.

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