ArticleJournal of neuroinflammation2018
Chorioamnionitis, neuroinflammation, and injury: timing is key in the preterm ovine fetus.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Postnatal Nutrition to Improve Brain Development in the Preterm Infant: A Systematic Review From Bench to Bedside.Frontiers in physiology · 2019Pooled it
- Effector and Activated T Cells Induce Preterm Labor and Birth That Is Prevented by Treatment with Progesterone.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- Stem cells redirect the neuroinflammatory trajectory of primed microglia in an ovine chorioamnionitis model.Brain, behavior, & immunity - health · 2026Article
- Mitochondrial dysfunction in neonatal brain injury: from molecular mechanisms to therapeutic interventions.Journal of translational medicine · 2026Review
- Modeling cerebral palsy in animals.Developmental medicine and child neurology · 2026Review
- Oxytocin Modulates Microglial IL-17-Linked Inflammatory Pathways Through the IL-6/COX-2.Life (Basel, Switzerland) · 2026Article
- A systematic scoring system to optimise the testing of neurotherapeutics in models of perinatal brain injury, with an applied case study of human umbilical-cord MSC.Journal of neuroinflammation · 2025Article
- The placenta as a window into neonatal brain injury.Seminars in perinatology · 2025Review
- The shifting landscape of the preterm brain.Neuron · 2025Review
- Interleukin-1 Receptor Antagonists Partially Inhibited Histological Injury but Not Tissue Inflammation in a Sheep Model of Pregnancy.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Human breast milk-derived exosomes attenuate lipopolysaccharide-induced activation in microglia.Journal of neuroinflammation · 2025Article
- Protective Effects of Early Neonatal Methylxanthine Treatment on Cognitive and Language Outcomes in Premature Infants with and without High-Risk Perinatal Factors.Developmental neuroscience · 2025Article
- Multipotent adult progenitor cells prevent functional impairment and improve development in inflammation driven detriment of preterm ovine lungs.Regenerative therapy · 2024Article
- How does fetal inflammatory response syndrome change fetal response to hypoxia? An experimental study in a fetal sheep model.Acta obstetricia et gynecologica Scandinavica · 2024Article
- Timed fetal inflammation and postnatal hypoxia cause cortical white matter injury, interneuron imbalances, and behavioral deficits in a double-hit rat model of encephalopathy of prematurity.Brain, behavior, & immunity - health · 2024Article
- Postnatal budesonide improved lung function in preterm lambs exposed to antenatal steroids and chorioamnionitis.Pediatric research · 2024Article
- The neural and cardiovascular effects of exposure of gram-positive bacterial inflammation in preterm fetal sheep.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Review
- Role of Microglial Modulation in Therapies for Perinatal Brain Injuries Leading to Neurodevelopmental Disorders.Advances in neurobiology · 2024Review
- Antenatal Ureaplasma infection induces ovine small intestinal goblet cell defects: a strong link with NEC pathology.Tissue barriers · 2023Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAntenatal infection (i.e., chorioamnionitis) is an important risk factor for adverse neurodevelopmental outcomes after preterm birth. Destructive and developmental disturbances of the white matter are hallmarks of preterm brain injury. Understanding the temporal effects of antenatal infection in relation to the onset of neurological injury is crucial for the development of neurotherapeutics for preterm infants. However, these dynamics remain unstudied.
methodsTime-mated ewes were intra-amniotically injected with lipopolysaccharide at 5, 12, or 24 h or 2, 4, 8, or 15 days before preterm delivery at 125 days gestational age (term ~ 150 days). Post mortem analyses for peripheral immune activation, neuroinflammation, and white matter/neuronal injury were performed. Moreover, considering the neuroprotective potential of erythropoietin (EPO) for perinatal brain injury, we evaluated (phosphorylated) EPO receptor (pEPOR) expression in the fetal brain following LPS exposure.
resultsIntra-amniotic exposure to this single bolus of LPS resulted in a biphasic systemic IL-6 and IL-8 response. In the developing brain, intra-amniotic LPS exposure induces a persistent microgliosis (IBA-1 immunoreactivity) but a shorter-lived increase in the pro-inflammatory marker COX-2. Cell death (caspase-3 immunoreactivity) was only observed when LPS exposure was greater than 8 days in the white matter, and there was a reduction in the number of (pre) oligodendrocytes (Olig2- and PDGFRα-positive cells) within the white matter at 15 days post LPS exposure only. pEPOR expression displayed a striking biphasic regulation following LPS exposure which may help explain contradicting results among clinical trials that tested EPO for the prevention of preterm brain injury.
conclusionWe provide increased understanding of the spatiotemporal pathophysiological changes in the preterm brain following intra-amniotic inflammation which may aid development of new interventions or implement interventions more effectively to prevent perinatal brain damage.
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