ArticleJournal of neuroinflammation2015
Early inflammatory mediator gene expression in two models of traumatic brain injury: ex vivo cortical slice in mice and in vivo cortical impact in piglets.
Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- The utilization of small non-mammals in traumatic brain injury research: A systematic review.CNS neuroscience & therapeutics · 2021Pooled it
- Early measurement of interleukin-10 predicts the absence of CT scan lesions in mild traumatic brain injury.PloS one · 2018Trial
- Review
- Circulating CD24/Siglec-10 biomarkers predict post-resuscitation outcomes in a cardiac arrest cohort.Scientific reports · 2025Article
- Backpack-mediated anti-inflammatory macrophage cell therapy for the treatment of traumatic brain injury.PNAS nexus · 2024Article
- Article
- Glial immune-related pathways mediate effects of closed head traumatic brain injury on behavior and lethality in Drosophila.PLoS biology · 2022Article
- Transcriptional Profiling in a Novel Swine Model of Traumatic Brain Injury.Neurotrauma reports · 2022Article
- Article
- Double-Injected Human Stem Cells Enhance Rehabilitation in TBI Mice Via Modulation of Survival and Inflammation.Molecular neurobiology · 2018Article
- Review
- Preventing inflammation inhibits biopsy-mediated changes in tumor cell behavior.Scientific reports · 2017Article
- Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection.Parasites & vectors · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe immunological response during the first 24 hours after traumatic brain injury (TBI) may be a critical therapeutic interval for limiting the secondary neuronal damage that is influenced by enhanced inflammatory mediator expression.
methodsTo gain further insight of the early injury response, we examined the expression of several inflammatory genes by real-time qPCR as a function of time or distance from injury in two distinct mammalian models: an ex vivo mouse cortical slice injury system and an in vivo piglet model of brain injury.
resultsInterleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), chemokine ligands 2 (CCL2), 3 (CCL3), 4 (CCL4), and prostaglandin-endoperoxide synthase 2 (PTGS2) mRNAs increased within 5 h after injury in mouse cortical slices. Chemokine and PTGS2 mRNAs remained elevated in slices at 24 h, whereas IL-1β and TNF-α expressions decreased from earlier peak levels. At 24 h after cortical injury in 1-month-old piglets, the expression of CCL2 mRNA was significantly increased in the lesion core and in the penumbra region. The expression of PTGS2, IL-1β, and TNF-α was variable among the piglets.
conclusionsThese in vitro and large animal models of cortical injury expand our understanding of the early timing and spread of the immunological response and can serve as preclinical systems to facilitate the discovery of therapeutic agents for TBI aimed at regulating inflammatory mediator expression.
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