ArticleJournal of neuroinflammation2014
The immune response after hypoxia-ischemia in a mouse model of preterm brain injury.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 69 citations in OpenAlex.
- Preconditioning and Posttreatment Strategies in Neonatal Hypoxic-Ischemic Encephalopathy: Recent Advances and Clinical Challenges.Molecular neurobiology · 2025Review
- Enteral plasma feeding improves gut function and immunity in piglets after birth asphyxia.Pediatric research · 2025Article
- Shared genetic features inference among hypoxia-ischemia diseases in the presence of heterogenous omics data based on a novel risk assessment method.Frontiers in genetics · 2025Article
- Review
- Review
- Increased glutamatergic synaptic transmission during development in layer II/III mouse motor cortex pyramidal neurons.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Alpha1-antitrypsin protects the immature mouse brain following hypoxic-ischemic injury.Frontiers in cellular neuroscience · 2023Article
- Periventricular Microglia Polarization and Morphological Changes Accompany NLRP3 Inflammasome-Mediated Neuroinflammation after Hypoxic-Ischemic White Matter Damage in Premature Rats.Journal of immunology research · 2023Article
- Effects of MgSOInternational journal of molecular sciences · 2022Article
- Temporal brain transcriptome analysis reveals key pathological events after germinal matrix hemorrhage in neonatal rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Review
- Peripheral immune cells and perinatal brain injury: a double-edged sword?Pediatric research · 2022Review
- Ambient Temperature Is Correlated With the Severity of Neonatal Hypoxic-Ischemic Brain Injury via Microglial Accumulation in Mice.Frontiers in pediatrics · 2022Article
- White Matter Injury in Preterm Infants: Pathogenesis and Potential Therapy From the Aspect of the Gut-Brain Axis.Frontiers in neuroscience · 2022Review
- The Role of Extracellular Vesicles in the Developing Brain: Current Perspective and Promising Source of Biomarkers and Therapy for Perinatal Brain Injury.Frontiers in neuroscience · 2021Review
- Review
- Experimentally Induced Sepsis Causes Extensive Hypomyelination in the Prefrontal Cortex and Hippocampus in Neonatal Rats.Neuromolecular medicine · 2020Article
- Complement C3a induces axonal hypomyelination in the periventricular white matter through activation of WNT/β-catenin signal pathway in septic neonatal rats experimentally induced by lipopolysaccharide.Brain pathology (Zurich, Switzerland) · 2020Article
- Vancomycin Is Protective in a Neonatal Mouse Model ofAntimicrobial agents and chemotherapy · 2020Article
- N-acetylcysteine inhibits bacterial lipopeptide-mediated neutrophil transmigration through the choroid plexus in the developing brain.Acta neuropathologica communications · 2020Article
- The Association Study ofFrontiers in neuroscience · 2020Article
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Authors and funding
12 authors at 6 institutions in 4 countries.
Funding
Abstract
backgroundPreterm brain injury consists primarily of periventricular leukomalacia accompanied by elements of gray-matter injury, and these injuries are associated with cerebral palsy and cognitive impairments. Inflammation is believed to be an important contributing factor to these injuries. The aim of this study was to examine the immune response in a postnatal day (PND) 5 mouse model of preterm brain injury induced by hypoxia-ischemia (HI) that is characterized by focal white and gray-matter injury.
methodsC57Bl/6 mice at PND 5 were subjected to unilateral HI induced by left carotid artery ligation and subsequent exposure to 10% O2 for 50 minutes, 70 minutes, or 80 minutes. At seven days post-HI, the white/gray-matter injury was examined. The immune responses in the brain after HI were examined at different time points after HI using RT-PCR and immunohistochemical staining.
resultsHI for 70 minutes in PND 5 mice induced local white-matter injury with focal cortical injury and hippocampal atrophy, features that are similar to those seen in preterm brain injury in human infants. HI for 50 minutes resulted in a small percentage of animals being injured, and HI for 80 minutes produced extensive infarction in multiple brain areas. Various immune responses, including changes in transcription factors and cytokines that are associated with a T-helper (Th)1/Th17-type response, an increased number of CD4+ T-cells, and elevated levels of triggering receptor expressed on myeloid cells 2 (TREM-2) and its adaptor protein DNAX activation protein of 12 kDa (DAP12) were observed using the HI 70 minute preterm brain injury model.
conclusionsWe have established a reproducible model of HI in PND 5 mice that produces consistent local white/gray-matter brain damage that is relevant to preterm brain injury in human infants. This model provides a useful tool for studying preterm brain injury. Both innate and adaptive immune responses are observed after HI, and these show a strong pro-inflammatory Th1/Th17-type bias. Such findings provide a critical foundation for future studies on the mechanism of preterm brain injury and suggest that blocking the Th1/Th17-type immune response might provide neuroprotection after preterm brain injury.
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