Cytokine mapping of sera from women with preeclampsia and normal pregnancies

Jonsson, Yvonne; Rubér, Marie; Matthiesen, Leif; Berg, Göran; Nieminen, Katri; Sharma, Surendra; Ernerudh, Jan; Ekerfelt, Christina

doi:10.1016/j.jri.2005.10.007

Cited by 233 publications

(180 citation statements)

References 28 publications

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“…The mean serum IL-10 level in patients with eclampsia in this study was significantly lower than levels found in normal pregnant and nonpregnant controls.This was different from the study of Jonsson et al, [14] where levels of IL-10 did not differ between women with preeclampsia and normal pregnancies. In humans the release of IL-10 by TH2 cells, macrophages and B cells has been shown to be up-regulated by circulating TNF-α [20] with IL-10 having the ability to suppress the synthesis of pro-inflammatory cytokines from T cells, leucocytes and macrophages and effectively down-regulate the inflammatory response.…”

Section: Discussioncontrasting

confidence: 99%

“…The results of this study showed that pro-inflammatory cytokine TNF-α level were present in higher concentrations in women with eclampsia compared to control nonpregnant women, though the increase was not specific for eclampsia with similar values being found in normal healthy pregnant controls. Increased production of pro-inflammatory cytokines such as IL-6 and TNF-α are known to occur in normal pregnancy, pregnant women in labor and in eclampsia [8,14]. The results of this study confirm these findings though the underlying mechanism for the cytokinaemia might differ.…”

Section: Discussionsupporting

confidence: 85%

“…Intrauterine fetal death was observed in 16 (50%) patients and a roughly equal number of patients (14) had live births ( Table 3). The outcome of delivery was unknown in 2 (6%) patients who were taken out of the ABU Teaching Hospital due to financial constraints.…”

Section: Demographic and Clinical Features In Eclampsiamentioning

confidence: 99%

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Serum cytokine levels and T lymphocyte subsets in pregnant women with eclampsia

Musa¹,

Onyemelukwe²,

Olatunji³

et al. 2012

OJI

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Background: Eclampsia, defined as the occurrence during pregnancy of hypertension, oedema, proteinuria and/or other neurologic abnormalities, causes substantial morbidity and mortality for both mother and foetus. However, its aetiology is largely unknown. Genetic and immune factors may play a role including a reduced maternal response to paternal antigen and an altered adaptation of the maternal immune system to the foetus. Methods: Participants consisted of pregnant women with and without a diagnosis of eclampsia (N = 20, each group), and normal healthy nonpregnant controls (N = 18). Women with smear positive malaria or clinical infections were excluded. Serum levels of TNFα and IL-10 were assayed by ELISA. T lymphocyte subsets of pregnant patients with and without eclampsia were also studied by direct immunofluorescence using monoclonal antibodies and compared with the control group of 18 normal healthy nonpregnant women (NHC). Results: Eclampsia was associated with significantly lower mean serum IL-10 levels compared to normal pregnant and nonpregnant controls. Levels of the pro-inflammatory cytokine TNFα were higher in pregnant women with and without eclampsia, compared to control nonpregnant women. Further differences on serum cytokine levels were observed in the significantly increasing ratio of IL-10 to TNFα from nonpregnant controls to normal pregnant women and to pregnant women with eclampsia. The mean values of CD3+ and CD4+ positive lymphocytes was significantly decreased in patients with eclampsia (p < 0.05) in this study compared to pregnant controls. Similarly, CD3+ and CD4+ T cells were further decreased in eclampsia and pregnant controls compared to nonpregnant controls (p < 0.05). A decreasing CD4/CD8 ratio was observed from non-pregnant to pregnant controls and to patients with eclampsia buttressing an increase in CD8+ cells in eclampsia and pregnancy compared to controls. Conclusions: While a pro-inflammatory immune milieu during pregnancy complicated with eclampsia was demonstrated, the presence of eclampsia was not associated with further cytokine differences.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 85%

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Serum cytokine levels and T lymphocyte subsets in pregnant women with eclampsia

Musa¹,

Onyemelukwe²,

Olatunji³

et al. 2012

OJI

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“…50 Compared with plasma from control women, the plasma of preeclamptic patients is also reported to contain elevated levels of placental debris 12,13 and reactive oxygen species, 14 -16 as well as augmented levels of proinflammatory cytokines such as TNF-␣, 16 -19,25 soluble forms of the TNF receptor, 19,24,26 and interleukin-8. 16,20,21 These inflammatory mediators likely synergize with elevated plasma IL-6 levels to promote systemic vascular damage, particularly in the kidney, that results in the characteristic proteinuria and hypertension of the maternal syndrome of preeclampsia.…”

Section: Discussionmentioning

confidence: 99%

Preeclampsia-Related Inflammatory Cytokines Regulate Interleukin-6 Expression in Human Decidual Cells

Lockwood

Yen

Başar

et al. 2008

The American Journal of Pathology

142

100

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Preeclampsia, a common pregnancy disorder associated with an increase in systemic inflammation, is the leading cause of maternal and fetal morbidity and mortality throughout the world. It is associated with shallow extravillous trophoblast invasion of the decidua, leading to uteroplacental blood flow that is inadequate for the developing fetal-placental unit. In preeclamptic women, interleukin-6 (IL-6) levels in plasma, but not placenta, are elevated, prompting evaluation of the decidua as a potential source of this excess, circulating IL-6. The current study found significantly higher immunohistochemical staining for IL-6 in decidual cells from preeclamptic versus preterm, gestational age-matched control placentas. Proinflammatory cytokines associated with the genesis of preeclampsia (i.e., tumor necrosis factor-␣ and interleukin-1␤) enhanced IL-6 mRNA levels and increased secreted IL-6 levels in first trimester leukocytefree decidual cell incubations, as measured by real time quantitative RT-PCR , ELISA , and Western blotting. Therefore , decidual cell-derived IL-6 may contribute to excess circulating IL-6 levels that can promote both endothelial cell dysfunction (and subsequent vascular dysfunction) and the pathogenesis of preeclampsia whereas locally elevated IL-6 levels may contribute to an excess of decidual macrophages implicated in shallow extravillous trophoblast invasion of the decidua. Maternal-fetal interactions create a mild systemic inflammatory state exemplified by activation of both vascular endothelium and leukocytes that is most apparent in the third trimester of uncomplicated human pregnancies.

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“…A defect of deep placentation [9][10][11][12][13] is proposed to generate utero-placental ischemia [14][15][16], placental endoplasmic reticulum and oxidative stress [17][18][19][20][21][22], and subsequently systemic intravascular inflammation [23][24][25] and endothelial dysfunction [17,[26][27][28][29][30][31][32][33][34]. The circulating concentrations of pro-inflammatory cytokines, such as interleukin (IL)-1-b and tumor necrosis factor (TNF)-a [35][36][37][38][39], as well as other inflammatory mediators (such as IL-6) [36,[40][41][42] are typically elevated in patients with preeclampsia, although this is not a universal feature [43,44]. The placenta is essential for the development of preeclampsia, while the fetus is not [45][46][47].…”

Section: Introductionmentioning

confidence: 99%

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

Stampalija

Chaiworapongsa

Romero

et al. 2013

The Journal of Maternal-Fetal & Neonatal Medicine

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Objectives: Angiogenic/anti-angiogenic factors have emerged as one of the promising biomarkers for the prediction of preeclampsia. Since not all patients with preeclampsia can be identified by these analytes, the search for additional biomarkers continues. The soluble form of ST2 (sST2), a protein capable of binding to interleukin (IL)-33 and thus contributing to a Th1-biased immune response, has been reported to be elevated in maternal plasma of women with preeclampsia. The aims of this study were to examine: (1) differences in maternal plasma concentrations of sST2 and IL-33 between women diagnosed with preeclampsia and those having uncomplicated pregnancies; (2) the relationship between sST2, umbilical and uterine artery Doppler velocimetry, and the severity of preeclampsia; and (3) the performance of sST2 and angiogenic/anti-angiogenic factors in identifying patients with preeclampsia at the time of diagnosis. Methods: This cross-sectional study included women with preeclampsia (n ¼ 106) and women with an uncomplicated pregnancy (n ¼ 131). Plasma concentrations of sST2, IL-33, soluble vascular endothelial growth factor receptor (sVEGFR)-1, soluble endoglin (sEng) and placental growth factor (PlGF) were determined by enzyme linked immune sorbent assay. Area under the receiver operating characteristic curve (AUC) for the identification of preeclampsia was examined for each analyte. Results: (1) Patients with preeclampsia had a higher mean plasma concentrations of sST2 than those with an uncomplicated pregnancy (p50.0001), while no significant difference in the mean plasma concentration of IL-33 between the two groups was observed; (2) the magnitude of this difference was greater in early-onset, compared to late-onset disease, and in severe compared to mild preeclampsia; (3) sST2 plasma concentrations did not correlate with the results of uterine or umbilical artery Doppler velocimetry (p ¼ 0.7 and p ¼ 1, respectively) among women with preeclampsia; (4) sST2 correlated positively with plasma concentrations of sVEGFR1-1 and sEng (Spearman's Rho ¼ 0.72 and 0.63; each p50.0001), and negatively with PlGF (Spearman's Rho ¼ À0.56, p50.0001); and (5) while the AUC achieved by sST2 and angiogenic/anti-angiogenic factors in identifying women with preeclampsia at the time of diagnosis were non-significantly different prior to term (537 weeks of gestation), thereafter the AUC achieved by sST2 was significantly less than that achieved by angiogenic/anti-angiogenic factors. Conclusions: Preeclampsia is associated with increased maternal plasma concentrations of sST2. The findings that sST2 concentrations do not correlate with uterine or umbilical artery Doppler velocimetry in women with preeclampsia suggest that elevated maternal plasma sST2 concentrations in preeclampsia are not related to the increased impedance to flow in the uteroplacental circulation. The performance of sST2 in identifying preeclampsia at the time of diagnosis prior to 37 weeks of gestation was comparable to that of angiogenic/anti-angiogenic f...

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Cytokine mapping of sera from women with preeclampsia and normal pregnancies

Cited by 233 publications

References 28 publications

Serum cytokine levels and T lymphocyte subsets in pregnant women with eclampsia

Serum cytokine levels and T lymphocyte subsets in pregnant women with eclampsia

Preeclampsia-Related Inflammatory Cytokines Regulate Interleukin-6 Expression in Human Decidual Cells

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

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