Maternal and umbilical serum concentrations of granulocyte colony-stimulating factor and its messenger RNA during clinical chorioamnionitis

Yan, Li; Ohls, Robin K.; Rosa, Cesar; Shah, Mita; Richards, Douglas; Christensen, Robert D.

doi:10.1016/0029-7844(95)00189-x

Cited by 20 publications

(5 citation statements)

References 15 publications

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“…Therefore, the induction of necrotizing funisitis in an experimental animal model has the potential to simulate the severe form of neonatal injury. Overall, these data (7,20,21,22,23) support the notion that exacerbated inflammation by G-CSF and high-dose endotoxin causes substantial fetal lung and brain injury, as opposed to fetal pulmonary maturational or protective effects observed with low-dose IA endotoxin injections.…”

Section: Discussionsupporting

confidence: 65%

“…(7) suggested that fetal G-CSF pretreatment before activation in utero by an IA infusion is 100% effective to induce necrotizing funisitis. This assumption depends on the observation that preterm neonates born following chorioamnionitis had significantly higher umbilical cord G-CSF levels than those without chorioamnionitis (20) . Moreover, fetuses with fetal inflammatory syndrome were found to have high median fetal plasma G-CSF concentrations (21,22) .…”

Section: Discussionmentioning

confidence: 99%

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Inflammation-mediated fetal injury by maternal granulocyte-colony stimulating factor and high-dose intraamniotic endotoxin in the caprine model

Sezi̇k

Köker

Özmen

et al. 2019

tjod

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Objective: To define a novel experimental model with maternal intravenous (i.v.) granulocyte-colony stimulating factor (G-CSF) followed by a single- and high-dose of 20 mg intra-amniotic (IA) endotoxin to induce fetal brain injury in the preterm fetal goat. Materials and Methods: Pregnant goats (n=4) were given 50 microg/day G-CSF into the maternal jugular vein through gestational days 110-115 (term, 150 days). At gestational day 115, 20 mg of IA endotoxin was administered. Following preterm delivery at day 120 by cesarean section umbilical cord, fetal lung and brain tissues were harvested for histopathology, immunohistochemistry, and electron microscopy. Inflammatory markers were evaluated in the amniotic fluid and fetal plasma. Results: Necrotizing funisitis with abundant leukocyte infiltration and fetal brain injury was induced in all the fetuses in the experimental group. Conclusion: Maternal i.v. G-CSF for 5 days followed by 20 mg of IA endotoxin is a feasible caprine model to exacerbate intrauterine inflammation.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Inflammation-mediated fetal injury by maternal granulocyte-colony stimulating factor and high-dose intraamniotic endotoxin in the caprine model

Sezi̇k

Köker

Özmen

et al. 2019

tjod

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“…Preterm labor/birth is associated with a systemic pro-inflammatory response (8, 18, 79-87). Therefore, we determined whether treatment with RSG reduced the elevated systemic concentrations of cytokines/chemokines induced by LPS.…”

Section: Resultsmentioning

confidence: 99%

An M1-like Macrophage Polarization in Decidual Tissue during Spontaneous Preterm Labor That Is Attenuated by Rosiglitazone Treatment

Romero

Miller

et al. 2016

The Journal of Immunology

160

137

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Macrophages are implicated in the local inflammatory response that accompanies spontaneous preterm labor/birth; however, their role is poorly understood. We hypothesized that decidual macrophages undergo an M1 polarization during spontaneous preterm labor and that PPARγ activation via rosiglitazone would attenuate the macrophage-mediated inflammatory response, preventing preterm birth. Herein, we show that: 1) decidual macrophages undergo an M1-like polarization during spontaneous term and preterm labor; 2) M2-like macrophages are more abundant than M1-like macrophages in decidual tissue; 3) decidual M2-like macrophages are reduced in preterm pregnancies compared to term pregnancies, regardless of the presence of labor; 4) decidual macrophages express high levels of TNF and IL12, but low levels of PPARγ, during spontaneous preterm labor; 5) decidual macrophages from women who underwent spontaneous preterm labor display plasticity by M1↔M2 polarization in vitro; 6) incubation with rosiglitazone reduces the expression of TNF and IL12 in decidual macrophages from women who underwent spontaneous preterm labor; and 7) treatment with rosiglitazone reduces the rate of LPS-induced preterm birth and improves neonatal outcomes by reducing the systemic pro-inflammatory response in B6 mice and down-regulating mRNA and protein expression of NFκB, TNF, and IL10 in decidual and myometrial macrophages. In summary, we demonstrated that decidual M1-like macrophages are associated with spontaneous preterm labor, and that PPARγ activation via rosiglitazone can attenuate the macrophage-mediated pro-inflammatory response, preventing preterm birth and improving neonatal outcomes. These findings suggest that the PPARγ pathway is a new molecular target for future preventative strategies for spontaneous preterm labor/birth.

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“…Cytokine activity can also trigger other biological events, such as activation of the hypothalamo-pituitary adrenal (HPA) axis (31), and is associated with increases in oxidative stress (32). Furthermore, maternally generated cytokines may cross the placenta (33) and blood-brain barrier (34). In this review, we will focus mainly on the pro-inflammatory cytokine IL-6 since there is a relatively robust preclinical and clinical literature on a role of IL-6 in SZ, although other cytokines, such as TNF-alpha and IL-2, may be involved.…”

Section: Infection In Schizophreniamentioning

confidence: 99%

The Cytokine Model of Schizophrenia: Emerging Therapeutic Strategies

Girgis

Kumar

Brown

2014

Biological Psychiatry

117

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We discuss the rationale for a trial of a novel biologic immunotherapy in schizophrenia (SZ). Available antipsychotic treatments for SZ are often limited by partial effectiveness and significant side effects. Thus, the search for novel medications is of high priority. All current antipsychotics function primarily by blocking D2-type dopamine receptors. An emerging theory of SZ postulates disturbances of cytokines and inflammatory mediators (i.e., the cytokine model), possibly originating in part from infectious exposures. Cytokines are one of the most important components of the immune system that orchestrate the response to infectious and other exogenous insults. Preclinical models of SZ support a convergence between a role for certain cytokines in the pathophysiology of SZ and major neurochemical postulates of the disorder, including the dopamine and glutamate hypotheses. Furthermore, several cytokines are elevated in plasma in SZ, and Positron Emission Tomography (PET) studies have shown active inflammation in the brains of individuals with psychosis. Treatment studies of certain anti-inflammatory agents, such as celecoxib and aspirin, in patients with SZ have provided further support for neuroinflammation in this disorder. The recent development of approved biological therapies for autoimmune diseases provides us with new opportunities to directly target cytokine signaling as a novel treatment strategy in SZ. In addition, advances in imaging, immunology, and psychopharmacology have paved the way for utilizing measures of target engagement of neuroimmune components that would facilitate the identification of patient subgroups who are most likely to benefit from cytokine modulation.

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Maternal and umbilical serum concentrations of granulocyte colony-stimulating factor and its messenger RNA during clinical chorioamnionitis

Abstract: Serum G-CSF concentrations were elevated during clinical chorioamnionitis, and similar levels were found in maternal and cord serum. Because G-CSF mRNA levels were very low in cord mononuclear cells, the G-CSF in cord serum might be maternal in origin.

Cited by 20 publications

References 15 publications

Inflammation-mediated fetal injury by maternal granulocyte-colony stimulating factor and high-dose intraamniotic endotoxin in the caprine model

Inflammation-mediated fetal injury by maternal granulocyte-colony stimulating factor and high-dose intraamniotic endotoxin in the caprine model

An M1-like Macrophage Polarization in Decidual Tissue during Spontaneous Preterm Labor That Is Attenuated by Rosiglitazone Treatment

The Cytokine Model of Schizophrenia: Emerging Therapeutic Strategies

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