Evaluation of maternal systemic inflammatory response in preeclampsia

Mihu, Dan; Ciortea, Răzvan; Măluţan, Andrei Mihai; Mihaela, Carmen

doi:10.1016/j.tjog.2014.03.006

Cited by 83 publications

(62 citation statements)

References 54 publications

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“…47,48 Systemic inflammation can be rapidly activated by LPS administration in experimental models, which subsequently increases the levels of inflammatory cytokines (TNF-α or IL-1β) and oxygenfree radicals. 8,49 In the present study, we administered LPS to pregnant rats to promote the development of PE and found that the serum levels of IL-1β significantly increased in the PE group compared with the NP, NP+LPS and P groups. Furthermore, TNF-α levels also increased by 30% compared with the P group.…”

Section: The Effect Of Mgso 4 On the Pe And Seizure Modelsmentioning

confidence: 49%

“…1,8 PE has been found to involve the activation of a large number of white blood cells, 9 and inflammatory markers, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and C-reactive protein, were increased at least twofold in PE patients compared with non-pregnant patients. [8][9][10][11][12] (TNF)-a infusion and low-dose lipopolysaccharide (LPS) infusion have been used to establish animal models of PE by inducing systemic inflammation in pregnant rats. 10 Eclampsia is associated with the development of tonic-clonic seizures in PE patients.…”

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confidence: 99%

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Increased neuronal seizure activity correlates with excessive systemic inflammation in a rat model of severe preeclampsia

et al. 2016

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Preeclampsia (PE), one of the most common disorders of pregnancy, is characterized by hypertension and albuminuria. In severe cases, PE results in eclampsia-like seizures. Studies have suggested that severe PE is related to an exaggerated systemic inflammatory response, which may increase sensitivity to seizures. In the current study, we investigated whether the seizure activity of neurons was enhanced under excessive systemic inflammation. We also sought to determine whether MgSO could reduce the effects of systemic inflammation on seizure activity after electrical stimulation in a lipopolysaccharide (LPS)-induced model of PE. In addition to pregnancy outcomes, we analyzed biochemical parameters to ascertain whether our PE model was successful. Enzyme-linked immunosorbent assay analysis revealed that the levels of inflammatory cytokines (tumor necrosis factor (TNF)-α and interleukin (IL)-1β) were significantly higher in the LPS-treated rats than in the untreated rats. After electrical stimulation, behavioral assessments showed that the LPS-treated rats that were not treated with MgSO had the shortest latency period to develop a seizure and the longest seizure duration. The electroencephalographic (EEG) recordings in the hippocampus demonstrated that this group also had the highest EEG amplitude. MgSO treatment significantly decreased both TNF-α and IL-1β concentrations, increased the latency to develop a seizure, decreased the seizure duration and shortened the EEG amplitude. These results suggest that neuronal seizure activity and systemic inflammation are increased in severe PE. In addition, MgSO treatment reduced systemic inflammation and seizure severity. We conclude that excessive systemic inflammation in PE promotes eclampsia seizures, which can be attenuated by MgSO treatment.

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Section: The Effect Of Mgso 4 On the Pe And Seizure Modelsmentioning

confidence: 49%

mentioning

confidence: 99%

Increased neuronal seizure activity correlates with excessive systemic inflammation in a rat model of severe preeclampsia

et al. 2016

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“…Preeclampsia has been described by some as an exaggerated state of inflammation (Mihu et al 2015) and others have made the case that the endocrine profile of PE is similar to that of a non-healing wound (Bird et al 2013). In this section we will briefly review hormones of inflammation/wounding which have been described as altered in PE compared to normal pregnancy, and may have causative adverse effects on endothelial cell function.…”

Section: Hormones Of Preeclampsia-related Endothelial Dysfunctionmentioning

confidence: 99%

Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

Boeldt

Bird

2017

Journal of Endocrinology

249

152

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Maternal vascular adaptation to pregnancy is critically important in order to expand the capacity for blood flow through the uteroplacental unit to meet the needs of the developing fetus. Failure of the maternal vasculature to properly adapt can result in hypertensive disorders of pregnancy such as preeclampsia (PE). Herein, we review the endocrinology of maternal adaptation to pregnancy and contrast this with that of PE. Our focus is specifically on those hormones with directly impact endothelial cell function and dysfunction, as endothelial cell dysfunction is a hallmark of PE. A variety of growth factors and cytokines are present in normal vascular adaptation to pregnancy but have also been shown to be circulating at abnormal levels in PE pregnancies. Many of these factors promote endothelial dysfunction when present at abnormal levels by acutely inhibiting key Ca2+ signaling events and chronically promoting the breakdown of endothelial cell-cell contacts. Increasingly, our understanding of how the contributions of the placenta, immune cells, and the endothelium itself promote the endocrine milieu of PE is becoming more clear. We then describe in detail how the complex endocrine environment of PE effects endothelial cell function, why this has contributed to the difficulty in fully understanding and treating this disorder, and how a focus on signaling convergence points of many hormones may be a more successful treatment strategy.

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“…16 In addition, it is regulated by hypoxia in mature dendritic cells. 17 Preeclampsia is a disease characterized by elevated levels of proinflammatory cytokines, such as C-reactive protein, IL-6, and others [18][19][20][21] and dysregulated trophoblast differentiation. 22 Two recent studies using microarray analysis have revealed that TREM-1 is increased in preeclamptic placentas.…”

Section: Introductionmentioning

confidence: 99%

TREM-1 Expression Is Increased in Human Placentas From Severe Early-Onset Preeclamptic Pregnancies Where It May Be Involved in Syncytialization

2014

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Preeclampsia, a major cause of maternal and perinatal morbidity and mortality, is thought to be attributable to dysregulation of trophoblast invasion and differentiation. Microarray studies have shown that triggering receptor expressed on myeloid cells (TREM) 1, a cell surface molecule involved in the inflammatory response, is increased in preeclamptic placentas. The aim of this study was to determine the level of TREM-1 expression in severe early-onset preeclamptic placentas and its functional role in trophoblast differentiation. Placenta was obtained from women with severe early-onset preeclampsia (n ¼ 19) and gestationally matched preterm controls placentas (n ¼ 8). The TREM-1 expression was determined by quantitative reverse transcriptase polymerase chain reaction and Western blotting. The effect of TREM-1 small interfering RNA on cell fusion and differentiation was assessed in BeWo cells. The effect of oxygen tension on TREM-1 levels, in basal or forskolin-treated BeWo cells, was also assessed. The TREM-1 was localized to the syncytiotrophoblast layer, and TREM-1 messenger RNA and protein expression was significantly increased in preeclamptic placentas. The BeWo cells treated with forskolin were associated with increased TREM-1 expression. The TREM-1 knockdown inhibited forskolin-induced expression of the differentiation marker b-human chorionic gonadotropin but had no effect on the cell-fusion marker E-cadherin. The increase in TREM-1 expression in BeWo cells treated with forskolin during normoxic conditions was reduced in forskolin-treated cells under hypoxic conditions. In conclusion, TREM-1 is increased in preeclamptic placentas and by forskolin treatment. Knockdown of TREM-1 by RNA interference inhibits cell differentiation but has no effect on cell-cell fusion. Finally, we show that TREM-1 upregulation is attenuated under hypoxic conditions in which cell differentiation is impaired.

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Evaluation of maternal systemic inflammatory response in preeclampsia

Abstract: In preeclampsia, there is an increased systemic inflammatory response compared to normal pregnancy, which can influence fetal status at birth.

Cited by 83 publications

References 54 publications

Increased neuronal seizure activity correlates with excessive systemic inflammation in a rat model of severe preeclampsia

Increased neuronal seizure activity correlates with excessive systemic inflammation in a rat model of severe preeclampsia

Vascular adaptation in pregnancy and endothelial dysfunction in preeclampsia

TREM-1 Expression Is Increased in Human Placentas From Severe Early-Onset Preeclamptic Pregnancies Where It May Be Involved in Syncytialization

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