Maternal peripheral blood leukocytes in normal and pre‐eclamptic pregnancies

Dadelszen, Peter von; Wilkins, T; Redman, Christopher W.G.

doi:10.1111/j.1471-0528.1999.tb08327.x

Cited by 58 publications

(42 citation statements)

References 25 publications

(27 reference statements)

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“…There was no significant change in abundance of any of the subunits investigated (densitometry for control resting cells, PMAstimulated control cells, preeclamptic resting cells, PMAstimulated preeclamptic cells, respectively for the different subunits:p47 phox: 1.00Ϯ0. 24 24; PϭN/S for all comparisons using the repeatedmeasures GLM procedure).…”

Section: Resultsmentioning

confidence: 99%

NADPH Oxidase Activity in Preeclampsia With Immortalized Lymphoblasts Used as Models

et al. 2003

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Abstract-Upon activation, neutrophils release reactive oxygen species that are believed to contribute to the widespread manifestation of preeclampsia. Neutrophils have an NADPH oxidase enzyme that catalyzes the production of reactive oxygen species. Little is known about the manifestations of the activated response and the upstream signaling pathways that regulate this process in preeclampsia. It is hypothesized that genetic factors may contribute to the release of reactive oxygen species and consequently the pathophysiology of the disease. We used Epstein-Barr virus-immortalized lymphoblasts from third-trimester, preeclamptic, postpartum preeclamptic women and their respective control subjects to assess NADPH oxidase-mediated reactive oxygen species production by using luminol-derived chemiluminescence and dihydrorhodamine-123 fluorescence. There was no effect of pregnancy status on the lymphoblast phorbol ester-stimulated luminol chemiluminescence area under the curve. However, lymphoblasts from preeclamptic patients had significant elevation of the lymphoblast phorbol ester-stimulated luminol area under the curve (F statistic 10.922, PϽ0.002). Similar findings were evident with dihydrorhodamine-123. No differences were revealed between preeclamptic and control cells when measuring the abundance of the phox proteins using Western blotting. Studies with genistein and tyrphostin implicated tyrosine kinase-dependent mechanisms in the control of NADPH oxidaseassociated increased reactive oxygen species production in preeclampsia. These data show that preeclampsia is associated with a predisposition to increased agonist-stimulated NADPH oxidase-mediated reactive oxygen species production. The enhancement of reactive oxygen species generation may be important in mediating the endothelial dysfunction seen in preeclampsia.

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Section: Resultsmentioning

confidence: 99%

NADPH Oxidase Activity in Preeclampsia With Immortalized Lymphoblasts Used as Models

et al. 2003

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“…[22][23][24] We chose to study neutrophils because they play a key role in innate immune defence 25 and there is evidence of their role in pre-eclampsia. 3,22,26,27 In addition, neutrophils express extracellular receptors, TLR2 and TLR4, and the intracellular cryopyrin inflammasome, which are crucial to inflammatory cytokine production. [28][29][30] Figure 1.…”

Section: Discussionmentioning

confidence: 99%

Toll‐like receptors 2 and 4 and the cryopyrin inflammasome in normal pregnancy and pre‐eclampsia

Xie¹,

Hu²,

Turvey

et al. 2009

BJOG

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Objective Pre-eclampsia involves a maternal inflammatory response that differs from both normal pregnancy and normotensive intrauterine growth restriction (IUGR). Our objective was to examine neutrophil Toll-like receptor (TLR), cryopyrin, nuclear factor-jB (NF-jB) subunit and interleukin-1b (IL-1b), and inflammatory cytokine profiles in women with preeclampsia or normotensive IUGR, as well as in normal pregnancy and non-pregnancy controls.Design and method A case-control study was performed. We examined the messenger RNA (mRNA) and protein expressions of TLR4 and TLR2, mRNA levels of cryopyrin, IL-1b, NF-jB subunits p50 and p65, as well as maternal serum inflammatory cytokine profiles (IL-2, IL-6, tumour necrosis factor-a [TNF-a], interferon-c [IFN-c] and IL-10) in women with and without pre-eclampsia using real-time reverse transcription polymerase chain reactions, flow cytometry and multiplex immunoassays.Setting A single tertiary maternity hospital in Vancouver, Canada.Population Women with early-onset pre-eclampsia (<34 weeks of gestation, n = 25), women with late-onset pre-eclampsia ( ‡34 +0 weeks of gestation, n = 25), women with normotensive IUGR (n = 25), women with normal pregnancy (n = 75) and non-pregnancy (n = 25) controls.Results Women with pre-eclampsia (as a single combined group of early-and late-onset, and particularly in women with earlyonset pre-eclampsia) had increased TLR2 and TLR4 mRNA and protein expressions elevated cryopyrin, NF-jB subunit, and IL-1b mRNA expression, and TNF-a:IL-10 and IL-6:IL-10 ratios compared with other groups.Conclusions These data suggest that TLRs and cryopyrin may modulate the innate immune response of the maternal syndrome of pre-eclampsia, and might also trigger the differential inflammatory response existing between early onset pre-eclampsia and normotensive IUGR.

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“…These cells could then be the source of increased inflammatory molecules. 64,65 Placental hormones including estrogen, 66 progesterone, 67 and human placental lactogen 68 have been suggested as the linkage, but in general, their role has been inconsistently supported. The role of aberrations of the renin-angiotensin system has been considered for many years.…”

Section: The Linkage Of Stages 1 Andmentioning

confidence: 99%

Preeclampsia

2005

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Abstract-Preeclampsia is a pregnancy complication with serious consequences for mother and infant. The disorder is diagnosed by gestational hypertension and proteinuria but is far more than pregnancy induced hypertension. Preeclampsia is proposed to occur in 2 stages. Key Words: preeclampsia Ⅲ hypertension, pregnancy Ⅲ oxidative stress Ⅲ endothelium P reeclampsia is a pregnancy complication recognized by new-onset gestational hypertension and proteinuria (see definitions below). The disorder affects both mothers and their infants. Once the disease is evident clinically, it can be cured only by delivery. In developed countries, surveillance for preeclampsia through prenatal care allows for early identification and intervention via delivery. This management has changed little in the last 100 years, and it is very effective at reducing maternal mortality. However, maternal morbidity remains great with preeclampsia, which continues to be one of the leading causes for the admission of pregnant women to intensive care units in the developed world. 1 Furthermore, fetal mortality and morbidity is considerable, related to the effects of the disease on the fetus as well as prematurity. The indicated delivery of women to prevent the progression of preeclampsia is responsible for 15% of all preterm births. 2 In developing countries, where inadequate prenatal care limits preeclampsia surveillance, maternal mortality is common, accounting for 50 000 deaths yearly. 3 The hypertensive disorders of pregnancy include hypertension that antedates pregnancy, chronic hypertension, and gestational hypertension occurring uniquely during pregnancy. When the gestational hypertension is accompanied by new-onset proteinuria, the disorder is termed preeclampsia, and when not associated with proteinuria, transient hypertension of pregnancy. If the woman with chronic hypertension also manifests evidence of preeclampsia, this is classified chronic hypertension with superimposed preeclampsia. Eclampsia is the occurrence of seizures in women with preeclampsia. 4 These criteria have been extraordinarily useful to aid in recognizing pregnant women at risk. Greatest risk for mother and baby is present with preeclampsia, and the risk for chronic hypertensive pregnancy is primarily with superimposed preeclampsia. However, the attention to hypertension has, for many years, limited research attention to primarily mechanisms of hypertension. This has not been helpful. In the last 2 decades, appreciation that preeclampsia is a multisystemic syndrome characterized by vasoconstriction, metabolic changes, endothelial dysfunction, activation of the coagulation cascade, and increased inflammatory response, to mention only some of the organ systems involved, has redirected research. 5 As a result, progress in understanding the disorder has accelerated greatly, with attendant optimism for potentially effective treatments. 5 In this article, we consider this recent progress and its clinical implications.

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Maternal peripheral blood leukocytes in normal and pre‐eclamptic pregnancies

Cited by 58 publications

References 25 publications

NADPH Oxidase Activity in Preeclampsia With Immortalized Lymphoblasts Used as Models

NADPH Oxidase Activity in Preeclampsia With Immortalized Lymphoblasts Used as Models

Toll‐like receptors 2 and 4 and the cryopyrin inflammasome in normal pregnancy and pre‐eclampsia

Preeclampsia

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