ArticleCNS neuroscience & therapeutics2017
Impact of prenatal immune challenge on the demyelination injury during adulthood.
Article in CNS neuroscience & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Beyond TORCH: A narrative review of the impact of antenatal and perinatal infections on the risk of disability.Neuroscience and biobehavioral reviews · 2023Review
- Hypoxic preconditioning improves long-term functional outcomes after neonatal hypoxia-ischemic injury by restoring white matter integrity and brain development.CNS neuroscience & therapeutics · 2019Article
- Impact of prenatal immune challenge on the demyelination injury during adulthood.CNS neuroscience & therapeutics · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aimBrain inflammation is associated with several brain diseases such as multiple sclerosis (MS), a disease characterized by demyelination. Whether prenatal immune challenge affects demyelination-induced inflammation in the white matter during adulthood is unclear. In the present study, we used a well-established experimental model of focal demyelination to assess whether prenatal immune challenge affects demyelination-induced inflammation.
methodsPregnant rats were injected with either lipopolysaccharide (100 μg/kg, ip) or pyrogen-free saline. A 2 μL solution of the gliotoxin ethidium bromide (0.04%) was stereotaxically infused into the corpus callosum of adult male offspring. The extent of demyelination lesion was assessed using Luxol fast blue (LFB) staining. Oligodendrocyte precursor cells, mature oligodendrocytes, markers of cellular gliosis, and inflammation were monitored in the vicinity of the demyelination lesion area.
resultsPrenatal lipopolysaccharide reduced the size of the demyelination lesion during adulthood. This reduced lesion was associated with enhanced density of mature oligodendrocytes and reduced density of microglial cells in the vicinity of the demyelination lesion. Such reduction in microglial cell density was accompanied by a reduced activation of the nuclear factor κB signaling pathway.
conclusionThese data strongly suggest that prenatal immune challenge dampens the extent of demyelination during adulthood likely by reprogramming the local brain inflammatory response to demyelinating insults.
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