The Neutrophil and Preeclampsia

Clark, Peter; Boswell, Fiona; Ia, Greer

doi:10.1055/s-2007-1016253

Cited by 77 publications

(52 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…28). Preeclampsia, a human pregnancy-related disorder, has been also associated with neutrophil activation (29,30) and with delay of neutrophil apoptosis (31) as sources of the high level of oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

NADPH Oxidase-dependent Oxidation and Externalization of Phosphatidylserine during Apoptosis in Me2SO-differentiated HL-60 Cells

Arroyo

Modrianský²,

Serinkan³

et al. 2002

Journal of Biological Chemistry

128

103

View full text Add to dashboard Cite

Resolution of inflammation requires clearance of activated neutrophils by phagocytes in a manner that protects adjacent tissues from injury. Mechanisms governing apoptosis and clearance of activated neutrophils from inflamed areas are still poorly understood. We used dimethylsulfoxide-differentiated HL-60 cells showing inducible oxidase activity to study NADPH oxidase-induced apoptosis pathways typical of neutrophils. Activation of the NADPH oxidase by phorbol myristate acetate caused oxidative stress as shown by production of superoxide and hydrogen peroxide, depletion of intracellular glutathione, and peroxidation of all three major classes of membrane phospholipids, phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine. In addition, phorbol myristate acetate stimulation of the NADPH oxidase caused apoptosis, as evidenced by apoptosis-specific phosphatidylserine externalization, increased caspase-3 activity, chromatin condensation, and nuclear fragmentation. Neutrophils aid host defense by killing invading microorganisms through production of highly reactive oxygen species (ROS) 1 generated by activation of the NADPH oxidase complex. When released inappropriately into the extracellular milieu, these ROS can cause persistent inflammation and considerable damage to the surrounding, healthy tissues. To prevent calamitous release of ROS, macrophages remove excess activated neutrophils from an inflammatory site in a regulated way, through processes that ensure swift resolution of inflammation yet make provision for neutrophils to fulfill their microbicidal function. Phagocytic cells carry out this clearance by recogniz-

show abstract

Section: Discussionmentioning

confidence: 99%

NADPH Oxidase-dependent Oxidation and Externalization of Phosphatidylserine during Apoptosis in Me2SO-differentiated HL-60 Cells

Arroyo

Modrianský²,

Serinkan³

et al. 2002

Journal of Biological Chemistry

128

103

View full text Add to dashboard Cite

show abstract

“…These include cytokines, TNF␣ in particular, 77 activated neutrophils, monocytes or platelets, 78 stable products of lipid peroxidation, 79 syncytiotrophoblast fragments and antibodies. The antibodies suggested include autoantibodies to endothelial cells 80 and more specifically autoantibodies to the angiotensin (AT 1 ) receptor 44 that are capable of activating the receptor.…”

Section: Effects On Ex Vivo Vesselsmentioning

confidence: 99%

Hypertension in pregnancy

Pipkin

Roberts

2000

J Hum Hypertens

View full text Add to dashboard Cite

Hypertension arising during pregnancy remains one of the two most frequently-cited causes of maternal death in the UK. In some cases, pregnancy is unmasking underlying hypertension, which manifests itself in later life. Pregnant women who develop de novo proteinuric hypertension (pre-eclampsia, PE) can share many risk factors with patients with the metabolic syndrome, such as obesity, dyslipidaemia and insulin resistance. However, more than half the women who develop PE remain normotensive thereafter. There is a genetic component(s) to the disease, but it is most improbable that there is a 'PE gene'. Rather, there are factors such as geneticallydetermined thrombophilias which are predisposers but not prerequisites. Impaired placentation is a feature, with inadequate invasion of the spiral arteries by syncytiotrophoblast and poor remodelling. However, similiar features are found in association with non-hypertensive

show abstract

“…Pathological edema is usually present. The pathophysiology of preeclampsia is associated with neutrophil activation, 4 oxidative stress, 5,6 and endothelial cell dysfunction. 7 Greer et al first reported that neutrophils were activated by measuring a significant increase in neutrophil elastase in the maternal circulation.…”

mentioning

confidence: 99%

Neutrophils Infiltrate Resistance-Sized Vessels of Subcutaneous Fat in Women With Preeclampsia

2004

View full text Add to dashboard Cite

Abstract-We examined if there is systemic vascular inflammation and neutrophil infiltration in women with preeclampsia.Resistance-sized vessels (10 to 200 m) of subcutaneous fat were evaluated from normal nonpregnant women, normal pregnant women, and preeclamptic women. Immunohistochemical staining was performed for: (1) interleukin-8 (IL-8), a potent neutrophil chemokine; (2) intercellular adhesion molecule-1 (ICAM-1; CD54), an endothelial cell adhesion molecule; and (3) CD66b, a neutrophil antigen. Vessels of preeclamptic patients had intense IL-8 staining in the endothelium and vascular smooth muscle, as compared with little or no staining for normal pregnant and normal nonpregnant patients. ICAM-1 was expressed on the endothelium of all patient groups. In preeclamptic patients, ICAM-1 was also expressed on vascular smooth muscle. Vessels of preeclamptic patients had significantly more CD66b staining of neutrophils than did normal pregnant or normal nonpregnant patients. There were significantly more vessels stained, more vessels with neutrophils flattened and adhered to endothelium, more vessels with neutrophils infiltrated into the intima, and more neutrophils per vessel. In conclusion, in women with preeclampsia, there was significant infiltration of neutrophils into maternal systemic vasculature associated with inflammation of the vascular smooth muscle indicated by increased expression of IL-8 and ICAM-1. Neutrophil infiltration provides a reasonable explanation for endothelial and vascular smooth muscle dysfunction in preeclampsia because neutrophils produce toxic substances, which may explain clinical symptoms.

show abstract

The Neutrophil and Preeclampsia

Cited by 77 publications

References 68 publications

NADPH Oxidase-dependent Oxidation and Externalization of Phosphatidylserine during Apoptosis in Me2SO-differentiated HL-60 Cells

NADPH Oxidase-dependent Oxidation and Externalization of Phosphatidylserine during Apoptosis in Me2SO-differentiated HL-60 Cells

Hypertension in pregnancy

Neutrophils Infiltrate Resistance-Sized Vessels of Subcutaneous Fat in Women With Preeclampsia

Contact Info

Product

Resources

About