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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Lipopolysaccharide-induced inflammation and perinatal brain injury
Xiaoyang Wang1, Catherine I Rousset, Henrik Hagberg
1Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy, Göteborg University, 40530 Göteborg, Sweden.
Insights
Fetal inflammation, often triggered by lipopolysaccharide (LPS), is a significant risk factor for infant brain injury. Early exposure increases vulnerability to later neurological damage, highlighting inflammation
Area of Science:
- Neuroscience
- Neonatal research
- Inflammation studies
Background:
- Energy failure and infections are key risk factors for infant brain injury.
- Lipopolysaccharide (LPS) exposure and its interactions with other events are critical in neonatal brain development.
- Understanding fetal and neonatal inflammation's impact on the brain is crucial for preventing long-term neurological deficits.
Purpose of the Study:
- To review experimental studies on the effects of lipopolysaccharide (LPS) exposure on fetal and neonatal brain development.
- To investigate the interaction between LPS exposure and other risk factors for brain injury.
- To identify the primary predictors of brain lesions in infants.
Main Methods:
- Review of experimental studies involving fetal or neonatal exposure to lipopolysaccharide (LPS).
- Analysis of cerebral cytokine response and white matter lesions following direct and indirect LPS administration.
- Assessment of brain sensitivity to hypoxic/ischaemic events after antenatal and neonatal LPS exposure.
Main Results:
- Intracerebral LPS injections trigger significant cerebral cytokine responses and white matter lesions.
- Intravenous fetal LPS exposure causes white matter lesions and inflammatory cell activation.
- Indirect fetal LPS exposure (intracervical, intrauterine, maternal) reduces oligodendrocyte/myelin markers without macroscopic lesions.
- Both antenatal and neonatal LPS exposure heighten brain susceptibility to hypoxic/ischaemic insults later in life.
Conclusions:
- Fetal inflammation is the most potent predictor of brain lesions in infants.
- LPS-induced fetal inflammation significantly impacts neonatal brain development and long-term neurological outcomes.
- Experimental models demonstrate a clear link between inflammatory insults and white matter injury in developing brains.
Abstract:
Both energy failure and infections are important risk factors for brain injury in term and preterm infants. In this review we focus on recent experimental studies that have examined the effects of lipopolysaccharide (LPS) exposure to the fetus or neonate and the interaction of LPS with other events. Intracerebral LPS injections induce a marked cerebral cytokine response and prominent white matter lesions. LPS administered intravenously to the fetus also induces gross lesions, which are mainly localised to the white matter and are accompanied by activation of inflammatory cells. Cerebral effects following fetal LPS exposure via more distant routes, such as intracervical, intrauterine or maternal LPS administration, are characterised by reductions in oligodendrocyte or myelin markers without macroscopic lesions being evident. Both antenatal and neonatal LPS exposures increase the sensitivity of the brain to subsequent hypoxic/ischaemic events, even in adulthood. These studies suggest that fetal inflammation is the strongest predictor of brain lesions.
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