Abstract
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.
Highlights
Fetoplacental inflammation secondary to intra-amniotic (IA) microbial colonization and subclinical chorioamnionitis provide a basis for the development of preterm birth and cerebral palsy (CP) by preferentially affecting the fetal brain tissue
granulocyte-colony stimulating factor (G-CSF) for 5 days followed by 20 mg of IA endotoxin is a feasible caprine model to exacerbate intrauterine inflammation
We aim to define our experience with intravenous (i.v.) recombinant (G-CSF) administrations for 5 days followed by a single-dose of 20 mg of IA endotoxin to induce IA inflammation, necrotizing funisitis, and fetal brain/lung injury in the preterm goat model
Summary
Fetoplacental inflammation secondary to intra-amniotic (IA) microbial colonization and subclinical chorioamnionitis provide a basis for the development of preterm birth and cerebral palsy (CP) by preferentially affecting the fetal brain tissue. Increased number of experimental and clinical work previously focused on fetoplacental inflammation and fetal brain injury. Animal models to aggravate intrauterine inflammation were often required and used[1] Within this context, the preterm small ruminant (such as sheep and goat) models that exclusively used IA endotoxin were accepted as relatively suitable designs to induce fetal lung and brain injury[2,3]. We aim to define our experience with intravenous (i.v.) recombinant (G-CSF) administrations for 5 days followed by a single-dose of 20 mg of IA endotoxin to induce IA inflammation, necrotizing funisitis, and fetal brain/lung injury in the preterm goat model. We hypothesized that our novel and relatively simple experimental model that does not require chronic maternal or fetal instrumentation would be able to produce exacerbated inflammation in utero, at least to an extent of that observed in previous experiments[1,2,3,5,6,7]
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