Coordinated Regulation of Human Trophoblast Invasiveness by Macrophages and Interleukin 101

Renaud, Stephen J.; Macdonald-Goodfellow, Shannyn K.; Graham, Charles H.

doi:10.1095/biolreprod.106.055376

Cited by 55 publications

(41 citation statements)

References 45 publications

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“…This effect was blocked by an antibody against the TNF-␣ receptor, 35 whereas inhibition of extravillous cytotrophoblast invasiveness by lipopolysaccharide-activated macrophages was reversed by a TNF-␣ neutralizing antibody. 36 Mediating this process by decidual cells was indicated by our observations that macrophages incubated with conditioned medium from IL-1␤-treated first trimester human decidual cells inhibited extravillous cytotrophoblast invasion. A report from our laboratory was the first to demonstrate a preeclampsia-related increase in decidual dendritic cells.…”

Section: Discussionmentioning

confidence: 99%

The Implication of Aberrant GM-CSF Expression in Decidual Cells in the Pathogenesis of Preeclampsia

Huang

Zenclussen

Chen

et al. 2010

The American Journal of Pathology

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Preeclampsia is characterized by an exaggerated systemic inflammatory state as well as shallow placentation. In the decidual implantation site , preeclampsia is accompanied by an excessive number of both macrophages and dendritic cells as well as their recruiting chemokines, which have been implicated in the impairment of endovascular trophoblast invasion. Granulocyte-macrophage colony-stimulating factor is known to regulate the differentiation of both macrophages and dendritic cells, prompting both in vivo and in vitro evaluation of granulocyte-macrophage colony-stimulating factor expression in human decidua as well as in a mouse model of preeclampsia. This study revealed increased granulocyte-macrophage colony-stimulating factor expression levels in preeclamptic decidua. Moreover, both tumor necrosis factor-␣ and interleukin-1 ␤, cytokines that are implicated in the genesis of preeclampsia, markedly up-regulated granulocyte-macrophage colony-stimulating factor production in cultured first-trimester human decidual cells. The conditioned media of these cultures promoted the differentiation of both macrophages and dendritic cells from a monocyte precursor. Evaluation of a murine model of preeclampsia revealed that the decidua of affected animals displayed higher levels of immunoreactive granulocyte-macrophage colony-stimulating factor as well as increased numbers of both macrophages and dendritic cells when compared to control animals. Because granulocyte-macrophage colony-stimulating factor is a potent inducer of differentiation and activation of both macrophages and dendritic cells , these findings suggest that this factor plays a crucial role in the pathogenesis of preeclampsia. (Am J

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Section: Discussionmentioning

confidence: 99%

The Implication of Aberrant GM-CSF Expression in Decidual Cells in the Pathogenesis of Preeclampsia

Huang

Zenclussen

Chen

et al. 2010

The American Journal of Pathology

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“…Salinetreated rats were used as control animals. Levels of TNF-a were subsequently quantified by ELISA according to the manufacturer's instructions (Alpco Diagnostics, Salem, NH) (29,30).…”

Section: Determination Of Tnf-a Levels By Enzyme Immunoassaymentioning

confidence: 99%

Spontaneous Pregnancy Loss Mediated by Abnormal Maternal Inflammation in Rats Is Linked to Deficient Uteroplacental Perfusion

Renaud

Cotechini

Quirt

et al. 2011

The Journal of Immunology

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123

113

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Abnormal maternal inflammation during pregnancy is associated with spontaneous pregnancy loss and intrauterine fetal growth restriction. However, the mechanisms responsible for these pregnancy outcomes are not well understood. In this study, we used a rat model to demonstrate that pregnancy loss resulting from aberrant maternal inflammation is closely linked to deficient placental perfusion. Administration of LPS to pregnant Wistar rats on gestational day 14.5, to induce maternal inflammation, caused fetal loss in a dose-dependent manner 3–4 h later, and surviving fetuses were significantly growth restricted. Pregnancy loss was associated with coagulopathy, structural abnormalities in the uteroplacental vasculature, decreased placental blood flow, and placental and fetal hypoxia within 3 h of LPS administration. This impairment in uteroplacental hemodynamics in LPS-treated rats was linked to increased uterine artery resistance and reduced spiral arteriole flow velocity. Pregnancy loss induced by LPS was prevented by maternal administration of the immunoregulatory cytokine IL-10 or by blocking TNF-α activity after treatment with etanercept (Enbrel). These results indicate that alterations in placental perfusion are responsible for fetal morbidities associated with aberrant maternal inflammation and support a rationale for investigating a potential use of immunomodulatory agents in the prevention of spontaneous pregnancy loss.

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“…Decidual macrophages are at a high concentration around invading trophoblast and may have roles in phagocytosis, tissue remodelling, interacting with trophoblasts, as well as in antigen presentation and innate defence. Differentiation is required to develop the decidual macrophage phenotype, with the state of activation as well as their secretion of cytokines influencing EVT invasion (Renaud et al 2007). …”

Section: Cd16mentioning

confidence: 99%

Remodelling at the maternal–fetal interface: relevance to human pregnancy disorders

Cartwright¹,

Fraser²,

Leslie³

et al. 2010

Reproduction

238

144

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In human pregnancy, successful placentation and remodelling of the uterine vasculature require the integration of a number of stages, which are crucial for a healthy pregnancy. As the demands of the developing fetus for nutrients and oxygen increase, the capacity of the maternal blood vessels to supply this must be altered radically, with deficiencies in this process implicated in a number of dangerous pregnancy complications. The complex signalling networks that regulate these tightly co-ordinated events are becoming clearer as more studies of early pregnancy are performed. It is the aim of this review to draw together our knowledge of events that occur to facilitate a successful pregnancy ranging from the preparation for implantation, through the invasion and differentiation of the trophoblast and the regulation of these processes by other cells within the decidual environment, to the active role that the trophoblast and maternal immune cells play in facilitating the remodelling of the uterine spiral arteries. The events involved in a healthy pregnancy will then be compared to aberrant placentation and remodelling, which are characteristics of many pregnancy disorders, and recent advances in detection of abnormal placental development will also be discussed.

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Coordinated Regulation of Human Trophoblast Invasiveness by Macrophages and Interleukin 101

Cited by 55 publications

References 45 publications

The Implication of Aberrant GM-CSF Expression in Decidual Cells in the Pathogenesis of Preeclampsia

The Implication of Aberrant GM-CSF Expression in Decidual Cells in the Pathogenesis of Preeclampsia

Spontaneous Pregnancy Loss Mediated by Abnormal Maternal Inflammation in Rats Is Linked to Deficient Uteroplacental Perfusion

Remodelling at the maternal–fetal interface: relevance to human pregnancy disorders

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