Phenotypic and metabolic characteristics of monocytes and granulocytes in preeclampsia

Gervasi, Maria-Teresa; Chaiworapongsa, Tinnakorn; Pacora, Percy; Naccasha, Nihal; Yoon, Bo Hyun; Maymon, Eli; Romero, Roberto

doi:10.1067/mob.2001.117311

Cited by 176 publications

(164 citation statements)

References 21 publications

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“…Consequently, we propose the hypothesis that leakage of fluids and proteins could result in edema and proteinuria, conditions observed in women with preeclampsia. 41,42 The maternal vascular system undergoes an inflammatory process during preeclampsia, as evidenced by increased neutrophil activation [43][44][45][46] and vascular neutrophil infiltration. 6 -8 In the early phase of this study, we hypothesized that infiltrating neutrophils could affect expression of genes related to the extracellular matrix.…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Estrada-Gutiérrez

Cappello

Mishra

et al. 2011

The American Journal of Pathology

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This study was conducted to determine the following: (1) whether matrix metalloproteinase-1 (MMP-1) is increased in systemic vessels of preeclamptic women, (2) whether this increase might be mediated by neutrophils, and (3) whether MMP-1 could be responsible for vascular dysfunction. Omental arteries and plasma were collected from healthy pregnant and preeclamptic women. Omental arteries were evaluated for gene and protein expression of MMP-1, collagen type 1␣, tissue inhibitor of metalloproteinase-1, and vascular reactivity to MMP-1. Gene and protein expression levels were also evaluated in human vascular smooth muscle cells (VSMCs) co-cultured with activated neutrophils, reactive oxygen species, or tumor necrosis factor ␣. Vessel expression of MMP-1 and circulating MMP-1 levels were increased in preeclamptic women, whereas vascular expression of collagen or tissue inhibitor of metalloproteinase-1 were down-regulated or unchanged. In cultured VSMCs, the imbalance in collagen-regulating genes of preeclamptic vessels was reproduced by treatment with neutrophils, tumor necrosis factor ␣, or reactive oxygen species. Chemotaxis studies with cultured cells revealed that MMP-1 promoted recruitment of neutrophils via vascular smooth muscle release of interleukin-8. Furthermore, MMP-1 induced vasoconstriction via protease-activated receptor-1, whose expression was significantly increased in omental arteries of preeclamptic women and in VSMCs co-cultured with neutrophils. Collectively, these findings disclose a novel role for MMP-1 as a mediator of vasoconstriction and vascular dysfunction in preeclampsia.

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Section: Discussionmentioning

confidence: 99%

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Estrada-Gutiérrez

Cappello

Mishra

et al. 2011

The American Journal of Pathology

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“…Specifically, deportation of villous trophoblast debris directly into the maternal circulation [10][11][12]15 has been implicated in the genesis of the exaggerated intravascular maternal inflammatory response noted in patients with pre-eclampsia 13,14,[16][17][18] . However, whether trophoblast debris is generated through apoptosis or necrosis has not been determined [57][58][59] .…”

Section: Discussionmentioning

confidence: 99%

“…The placenta, but not the fetus, is required for the development of the disorder, as patients with classic 'hydatidiform moles' (without a fetus) can develop pre-eclampsia 2 . The mechanisms responsible for the genesis of the syndrome are poorly understood 3,4 , although roles for uteroplacental ischemia [5][6][7][8] , endothelial cell dysfunction 9 and exaggerated maternal inflammatory response to deported trophoblast have been proposed [10][11][12][13][14][15][16][17][18] .…”

Section: Introductionmentioning

confidence: 99%

Maternal serum of women with pre-eclampsia reduces trophoblast cell viability: evidence for an increased sensitivity to Fas-mediated apoptosis

Neale

Demasio

Illuzi

et al. 2003

The Journal of Maternal-Fetal & Neonatal Medicine

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“…from the ischemic placenta into the maternal circulation [1][2][3] . A predisposed host exposed to these agents may then develop endothelial dysfunction 4 , systemic intravascular inflammation 5,6 and the clinical syndrome of pre-eclampsia. It has been suggested that the circulating factors might cross the placental barrier into the fetal circulation.…”

Section: Introductionmentioning

confidence: 99%

Neonates born to pre-eclamptic mothers have a higher percentage of natural killer cells (CD3 - /CD56+16+) in umbilical cord blood than those without pre-eclampsia

White

Ahlstrand²

2003

DJMF

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Objective: Maternal endothelial dysfunction and intravascular inflammation have been implicated in the mechanisms of disease responsible for the clinical syndrome of pre-eclampsia. Recently, the activation of the innate limb of the immune response (neutrophils and monocytes) in the fetal circulation has been reported in neonates born to mothers with pre-eclampsia. Natural killer (NK) cells are identified morphologically as a subpopulation of lymphocytes, but functionally as one component of the innate immune system. NK cells participate in the control of viral or bacterial infection, regulation of hematopoiesis, production of cytokines and cytotoxicity of neoplastic cells. Accumulating evidence suggests that the innate system is required for mounting an adequate adaptive response. NK cells, originally defined as effector cells of the innate immune system, may also play a role as regulatory cells for the adaptive immune system. This study was designed to determine the proportion of the NK cell subset of lymphocytes in umbilical cord blood of neonates born to mothers with and without pre-eclampsia. Methods: A cross-sectional study including neonates of mothers with (n = 48) and those without pre-eclampsia (control group) (n = 72) was conducted. Pre-eclampsia was diagnosed in the presence of hypertension and proteinuria. The control group consisted of neonates (premature and term) with no evidence of acute inflammation within the extraplacental membranes (chorioamnionitis). Umbilical cord blood was collected at the time of delivery, and assayed using monoclonal antibodies for selective cluster differentiation (CD) antigens in order to determine the proportion of NK cells as a percentage of total lymphocytes. The immunophenotypic characteristic was determined using flow cytometry, and NK cells were identified by positivity of CD16 and CD56 without CD3 (CD3-/CD56+16+). Log transformation of the percentage of NK cells was performed. Parametric statistics were used for analysis. Multiple regression analysis was utilized to examine the contribution of potentially confounding factors on the proportion of NK cells. A p value of < 0.05 was considered statistically significant. Results: Neonates born to mothers with pre-eclampsia had a significantly higher percentage of NK cells (CD3-/CD56+16+) than those in the control group (pre-eclampsia, mean ± SD 17 ± 9% vs. control, mean ± SD 12 ± 7.5%; p = 0.001). Multiple regression analysis suggested that umbilical cord blood pH of < 7.2, labor with vaginal delivery and maternal pre-eclampsia were associated with an increased percentage of NK cells in umbilical cord blood. Conclusions: Pre-eclampsia is associated with a higher NK cell (CD3-/CD56+16+) subset of lymphocytes in umbilical cord blood than in the control group. This difference cannot be explained by fetal acidosis or the presence of labor.

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Phenotypic and metabolic characteristics of monocytes and granulocytes in preeclampsia

Cited by 176 publications

References 21 publications

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Maternal serum of women with pre-eclampsia reduces trophoblast cell viability: evidence for an increased sensitivity to Fas-mediated apoptosis

Neonates born to pre-eclamptic mothers have a higher percentage of natural killer cells (CD3 - /CD56+16+) in umbilical cord blood than those without pre-eclampsia

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