ArticleJournal of neuroinflammation2023
IL-1R1 signaling in TBI: assessing chronic impacts and neuroinflammatory dynamics in a mouse model of mild closed-head injury.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- PANoptosis In Microglia and Neurons Following Traumatic CNS Injury: A Systematic Review of Pathological Features and Therapeutic Implications.CNS neuroscience & therapeutics · 2026Pooled it
- Orchestrating neuroinflammation: A symphony of Interleukin-1 and cell type-specific Interleukin-1 receptor type 1 signaling in the brain.Brain behavior and immunity integrative · 2026Article
- The Dynamics of Neuroinflammation in Traumatic Brain Injury: Molecular Markers Useful for Establishing the Post-Traumatic Interval in Forensic Practice.International journal of molecular sciences · 2026Review
- Temporal and Spatial Patterns of Glial Activation After Unilateral Cortical Injury in Rats.Life (Basel, Switzerland) · 2026Article
- A Novel snoRNA, Gm24418 Attenuates Inflammation Injury After Acute TBI Through Regulating CCL2.Journal of inflammation research · 2026Article
- A single mild closed-head injury disrupts synaptic strength and promotes hippocampal hyperexcitability in mice.Brain communications · 2026Article
- CSF1R and IL1R1 inhibitors synergistically attenuate the early pathogenesis of traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Cytokines and related signaling pathways in traumatic brain injury.Frontiers in immunology · 2026Review
- Identification of IL1R1 as a potential key PANoptosis-related gene in myocardial ischemia-reperfusion injury using machine learning.Scientific reports · 2025Article
- DTX1 Modulates Microglial M1 Polarization and Exacerbates Neuroinflammation in Traumatic Brain Injury Model Rats through NF-κB/IRF5.Molecular neurobiology · 2025Article
- Exploration of biomaterial and stem cell-based strategies for promoting neuronal regeneration and creating engineered 3D in-vitro disease models.Journal of translational medicine · 2025Review
- Intranasal delivery of hypoxia-preconditioned extracellular vesicles derived from BMSCs alleviates neuroinflammation and brain dysfunction in TBI.Stem cell research & therapy · 2025Article
- Diffuse traumatic brain injury induced stimulator of interferons (STING) signaling in microglia drives cortical neuroinflammation, neuronal dysfunction, and impaired cognition.Journal of neuroinflammation · 2025Article
- Diffuse Traumatic Brain Injury Induced Stimulator of Interferons (STING) Signaling in Microglia Drives Cortical Neuroinflammation, Neuronal Dysfunction, and Impaired Cognition.Research square · 2025Article
- Astrocytic and microglial cell functions in neuroinflammatory diseases and their animal models.Frontiers in cellular neuroscience · 2025Review
- Inflammasomes at the crossroads of traumatic brain injury and post-traumatic epilepsy.Journal of neuroinflammation · 2024Review
- Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction.Journal of neuroinflammation · 2024Article
- Chronic immunosuppression across 12 months and high ability of acute and subacute CNS-injury biomarker concentrations to identify individuals with complicated mTBI on acute CT and MRI.Journal of neuroinflammation · 2024Article
- Correction : IL-1R1 signaling in TBI: assessing chronic impacts and neuroinflammatory dynamics in a mouse model of mild closed-head injury.Journal of neuroinflammation · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Neuroinflammation contributes to secondary injury cascades following traumatic brain injury (TBI), with alternating waves of inflammation and resolution. Interleukin-1 (IL-1), a critical neuroinflammatory mediator originating from brain endothelial cells, microglia, astrocytes, and peripheral immune cells, is acutely overexpressed after TBI, propagating secondary injury and tissue damage. IL-1 affects blood-brain barrier permeability, immune cell activation, and neural plasticity. Despite the complexity of cytokine signaling post-TBI, we hypothesize that IL-1 signaling specifically regulates neuroinflammatory response components. Using a closed-head injury (CHI) TBI model, we investigated IL-1's role in the neuroinflammatory cascade with a new global knock-out (gKO) mouse model of the IL-1 receptor (IL-1R1), which efficiently eliminates all IL-1 signaling. We found that IL-1R1 gKO attenuated behavioral impairments 14 weeks post-injury and reduced reactive microglia and astrocyte staining in the neocortex, corpus callosum, and hippocampus. We then examined whether IL-1R1 loss altered acute neuroinflammatory dynamics, measuring gene expression changes in the neocortex at 3, 9, 24, and 72 h post-CHI using the NanoString Neuroinflammatory panel. Of 757 analyzed genes, IL-1R1 signaling showed temporal specificity in neuroinflammatory gene regulation, with major effects at 9 h post-CHI. IL-1R1 signaling specifically affected astrocyte-related genes, selectively upregulating chemokines like Ccl2, Ccl3, and Ccl4, while having limited impact on cytokine regulation, such as Tnfα. This study provides further insight into IL-1R1 function in amplifying the neuroinflammatory cascade following CHI in mice and demonstrates that suppression of IL-1R1 signaling offers long-term protective effects on brain health.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.