Expression of the placental cytokines tumor necrosis factor α, interleukin 1β, and interleukin 10 is increased in preeclampsia

Rinehart, Brian K.; Terrone, Dom A.; Lagoo‐Deenadayalan, Sandhya; Barber, William H.; b, Enatra A. Hale; Martin, James N.; Bennett, William A.

doi:10.1016/s0002-9378(99)70325-x

Cited by 210 publications

(124 citation statements)

References 21 publications

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“…But these effects may be very aggressive in severe preeclampsia, and the triggered value is determinative value for it, this may be cut off value. IL-1β is a known inducer of monocyte chemotactic protein (MCP) 1 expression [23] and its role in pathogenesis of preeclampsia was shown previously [15,24]. Our data was determined significantly higher blood levels of IL-1β in severe preeclampsia (P < 0.005) when compared to normal pregnant women, so this may be convinced of seriousness.…”

Section: Discussionsupporting

confidence: 70%

Maternal Inflammatory Response in Severe Preeclamptic and Preeclamptic Pregnancies

Bayram¹

2012

J Clin Gynecol Obstet

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Section: Discussionsupporting

confidence: 70%

Maternal Inflammatory Response in Severe Preeclamptic and Preeclamptic Pregnancies

Bayram¹

2012

J Clin Gynecol Obstet

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“…Serum IL-10 concentration is decreased in women with established pre-eclampsia 34 . All these interleukins are produced by placental tissues and represent both pro-and anti-inflammatory cytokines 35,36 . At 18 weeks of gestation, there seems to be no change in the circulating levels of these interleukins in women destined to develop pre-eclampsia.…”

Section: Medianmentioning

confidence: 99%

Absence of enhanced systemic inflammatory response at 18 weeks of gestation in women with subsequent pre-eclampsia

Djurovic¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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Objective To compare indicators of systemic inflammatory response in the second trimester in women who developed pre-eclampsia with normal pregnancies. Design Prospective nested case control study derived from a cohort of 2190 pregnant women. Blood samples were obtained at 18 weeks of gestation. The following inflammatory parameters were measured: tumour necrosis factor-a (TNF-a), plasminogen activator inhibitor-1 (PAI-1), interleukin-1h (IL-1h), IL-6, IL-10, microCRP and tissue factor (TF). Setting Institute of Medical Genetics, University of Oslo, and Department of Medical Genetics, Ullevål University Hospital and Departments of Obstetrics and Gynecology, Aker University Hospital, Oslo, Norway. Sample The cases were 71 women who subsequently developed pre-eclampsia. The controls were 71 healthy, pregnant women matched for age, parity and first trimester body mass index (BMI). Methods Venous blood was drawn from fasting subjects into 5 mL test tubes containing EDTA. Samples were analysed for inflammatory parameters : IL-1-h, IL-6, IL-10, TNF-a, PAI-1, TF (ELISA-technique) and CRP (latex-enhanced immunonephelometric assay), strictly according to the manufacturer's recommendation. Main outcome measures The matched case and control subjects were compared by the paired two-tailed Wilcoxon signed rank test. All P values were two-tailed and P < 0.05 was deemed statistically significant. Results We found no differences in plasma concentrations of PAI-1, IL-1h, IL-6, IL-10, microCRP, TNF-a or TF at 18 weeks of gestation between women who subsequently developed pre-eclampsia and matched control women. Conclusion In contrast to findings from women with overt pre-eclampsia, the present study indicates that there are no indications of intensified systemic inflammatory response at 18 weeks of gestation in women who later develop pre-eclampsia.

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“…Inversely, failure to mount a local inflammatory response in early or late gestation can also lead to adverse conditions, including miscarriages. Evidence shows that impaired inflammatory response is implicated in numerous female reproductive tract pathologies including menstrual disorders (Sales & Jabbour 2003), endometriosis-associated infertility (Gupta et al 2008), recurrent miscarriage (von Wolff et al 2000, Laird et al 2003, intrauterine growth restriction (Heyborne et al 1994), preeclampsia , Rinehart et al 1999) and preterm labor (Romero et al 2006. Infertility has an estimated global prevalence of 9% with >72 million infertile women worldwide (Boivin et al 2007), whereas preterm birth and preeclampsia, the two leading causes of perinatal mortality and morbidity, have an estimated prevalence of >11% (Blencowe et al 2013) and 3-5% (Ananth et al 2013 respectively.…”

Section: Introductionmentioning

confidence: 99%

Sterile inflammation and pregnancy complications: a review

Nadeau-Vallée¹,

Obari²,

Palacios³

et al. 2016

Reproduction

219

161

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Inflammation is essential for successful embryo implantation, pregnancy maintenance and delivery. In the last decade, important advances have been made in regard to endogenous, and therefore non-infectious, initiators of inflammation, which can act through the same receptors as pathogens. These molecules are referred to as damage-associated molecular patterns (DAMPs), and their involvement in reproduction has only recently been unraveled. Even though inflammation is necessary for successful reproduction, untimely activation of inflammatory processes can have devastating effect on pregnancy outcomes. Many DAMPs, such as uric acid, high-mobility group box 1 (HMGB1), interleukin (IL)-1 and cell-free fetal DNA, have been associated with pregnancy complications, such as miscarriages, preeclampsia and preterm birth in preclinical models and in humans. However, the specific contribution of alarmins to these conditions is still under debate, as currently there is lack of information on their mechanism of action. In this review, we discuss the role of sterile inflammation in reproduction, including early implantation and pregnancy complications. Particularly, we focus on major alarmins vastly implicated in numerous sterile inflammatory processes, such as uric acid, HMGB1, IL-1α and cell-free DNA (especially that of fetal origin) while giving an overview of the potential role of other candidate alarmins.Reproduction (2016) 152 R277-R292

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Expression of the placental cytokines tumor necrosis factor α, interleukin 1β, and interleukin 10 is increased in preeclampsia

Cited by 210 publications

References 21 publications

Maternal Inflammatory Response in Severe Preeclamptic and Preeclamptic Pregnancies

Maternal Inflammatory Response in Severe Preeclamptic and Preeclamptic Pregnancies

Absence of enhanced systemic inflammatory response at 18 weeks of gestation in women with subsequent pre-eclampsia

Sterile inflammation and pregnancy complications: a review

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