ArticleJournal of neuroinflammation2018
Persistent reduction in sialylation of cerebral glycoproteins following postnatal inflammatory exposure.
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 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- NEU1-Mediated Extracellular Vesicle Glycosylation in Alzheimer's Disease: Mechanistic Insights into Intercellular Communication and Therapeutic Targeting.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Sialylation as a checkpoint for inflammatory and complement-related retinal diseases.Frontiers in cellular neuroscience · 2025Review
- SerumBiomolecules · 2024Article
- Combined Effect of Maternal Separation and Early-Life Immune Activation on Brain and Behaviour of Rat Offspring.Biomolecules · 2024Article
- Changes in tissue proteinPNAS nexus · 2024Article
- Microglia Mediate Contact-Independent Neuronal Network Remodeling via Secreted Neuraminidase-3 Associated with Extracellular Vesicles.ACS central science · 2023Article
- Risk factors and postnatal biomarkers for acute placental inflammatory lesions and intrauterine infections in preterm infants.European journal of pediatrics · 2022Article
- The dynamic brain N-glycome.Glycoconjugate journal · 2022Review
- Review
- Article
- Complete spatial characterisation of N-glycosylation upon striatal neuroinflammation in the rodent brain.Journal of neuroinflammation · 2021Article
- Depolarization-dependent Induction of Site-specific Changes in Sialylation onMolecular & cellular proteomics : MCP · 2020Article
- Control of Innate Immunity by Sialic Acids in the Nervous Tissue.International journal of molecular sciences · 2020Review
- Decreased Immunoglobulin G Core Fucosylation, A Player in Antibody-dependent Cell-mediated Cytotoxicity, is Associated with Autoimmune Thyroid Diseases.Molecular & cellular proteomics : MCP · 2020Article
- Sialylation and Galectin-3 in Microglia-Mediated Neuroinflammation and Neurodegeneration.Frontiers in cellular neuroscience · 2020Review
- The role of the mucin-glycan foragingGut microbesArticle
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe extension of sepsis encompassing the preterm newborn's brain is often overlooked due to technical challenges in this highly vulnerable population, yet it leads to substantial long-term neurodevelopmental disabilities. In this study, we demonstrate how neonatal neuroinflammation following postnatal E. coli lipopolysaccharide (LPS) exposure in rat pups results in persistent reduction in sialylation of cerebral glycoproteins.
methodsMale Sprague-Dawley rat pups at postnatal day 3 (P3) were injected in the corpus callosum with saline or LPS. Twenty-four hours (P4) or 21 days (P24) following injection, brains were extracted and analyzed for neuraminidase activity and expression as well as for sialylation of cerebral glycoproteins and glycolipids.
resultsAt both P4 and P24, we detected a significant increase of the acidic neuraminidase activity in LPS-exposed rats. It correlated with significantly increased neuraminidase 1 (Neu1) mRNA in LPS-treated brains at P4 and with neuraminidases 1 and 4 at P24 suggesting that these enzymes were responsible for the rise of neuraminidase activity. At both P4 and P24, sialylation of N-glycans on brain glycoproteins decreased according to both mass-spectrometry analysis and lectin blotting, but the ganglioside composition remained intact. Finally, at P24, analysis of brain tissues by immunohistochemistry showed that neurons in the upper layers (II-III) of somatosensory cortex had a reduced surface content of polysialic acid.
conclusionsTogether, our data demonstrate that neonatal LPS exposure results in specific and sustained induction of Neu1 and Neu4, causing long-lasting negative changes in sialylation of glycoproteins on brain cells. Considering the important roles played by sialoglycoproteins in CNS function, we speculate that observed re-programming of the brain sialome constitutes an important part of pathophysiological consequences in perinatal infectious exposure.
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