ArticleInflammation2023
Interleukin 4 Reduces Brain Hyperexcitability after Traumatic Injury by Downregulating TNF-α, Upregulating IL-10/TGF-β, and Potential Directing Macrophage/Microglia to the M2 Anti-inflammatory Phenotype.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Neurons Die Not by One Hit, but by Signaling Convergence.Molecular neurobiology · 2026Review
- Single-nucleus brain transcriptomics reveals microglia dysfunction in multiple system atrophy.Nature communications · 2026Article
- Cytokines and related signaling pathways in traumatic brain injury.Frontiers in immunology · 2026Review
- Systemic Interleukin-4 Application Promotes Functional Recovery and Reprograms Neuroinflammatory and Molecular Responses after Spinal Cord Injury in Rats.Theranostics · 2026Article
- TNF-α in traumatic brain injury: a bidirectional effect in regulating neuroimmune and inflammatory responses.Cellular and molecular life sciences : CMLS · 2025Review
- From Adhesions to Conception: A Case Study on Platelet-Rich Plasma's Role in Gynecologic Recovery.Cureus · 2025Article
- Balancing Anti-Inflammation and Neurorepair: The Role of Mineralocorticoid Receptor in Regulating Microglial Phenotype Switching After Traumatic Brain Injury.CNS neuroscience & therapeutics · 2025Article
- Olfactory mucosa-mesenchymal stem cells with overexpressed Nrf2 modulate angiogenesis and exert anti-inflammation effect in an in vitro traumatic brain injury model.European journal of medical research · 2025Article
- Identifying pyroptosis-hub genes and immune infiltration in neonatal hypoxic-ischemic brain injury.Frontiers in immunology · 2025Article
- Biomaterials for Modulating the Immune Microenvironment in Rheumatoid Arthritis.BME frontiers · 2025Review
- Research progress on the role of inflammatory mediators in the pathogenesis of epilepsy.Ibrain · 2025Review
- Focus on P2X7R in microglia: its mechanism of action and therapeutic prospects in various neuropathic pain models.Frontiers in pharmacology · 2025Review
- Dual role of Lyz2-positive myeloid cells in traumatic brain injury: acute anti-inflammatory effects vs. chronic neurological deterioration.Frontiers in cellular neuroscience · 2025Article
- Macrophage Polarization: A Novel Target and Strategy for Pathological Scarring.Tissue engineering and regenerative medicine · 2024Review
- Administration of monophosphoryl lipid A shortly after traumatic brain injury blocks the following spatial and avoidance memory loss and neuroinflammation.Scientific reports · 2024Article
- Crosstalk Among Glial Cells in the Blood-Brain Barrier Injury After Ischemic Stroke.Molecular neurobiology · 2024Review
- Loss of Mitochondrial Tusc2/Fus1 Triggers a Brain Pro-Inflammatory Microenvironment and Early Spatial Memory Impairment.International journal of molecular sciences · 2024Article
- Interleukins in Epilepsy: Friend or Foe.Neuroscience bulletin · 2024Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage/microglia are activated after Traumatic brain injury (TBI), transform to inflammatory phenotype (M1) and trigger neuroinflammation, which provokes epileptogenesis. Interleukin-4 (IL-4) is a well-known drive of macrophage/microglia to the anti-inflammatory phenotype (M2). We tested effect of IL-4 on speed of epileptogenesis, brain expression of inflammatory and anti-inflammatory cytokines, and lesion size in TBI-injured male rats. Rats underwent TBI by Controlled Cortical Impact. Then 100 ng IL-4 was injected into cerebral ventricles. One day after TBI, pentylenetetrazole (PTZ) kindling started and development of generalized seizures was recorded. The lesion size, cell survival rate, TNF-α, TGF-β, IL-10, and Arginase1 (Arg1) was measured in the brain 6 h, 12 h, 24 h, 48 h, and 5 days after TBI. Astrocytes and macrophage/microglia activation/polarization was assessed by GFAP/Arg1 and Iba1/Arg1 immunostaining. TBI-injured rats were kindled by 50% less PTZ injections than control and sham-operated rats. IL-4 did not change kindling rate in sham-operated rats but inhibited acceleration of kindling rate in the TBI-injured rats. IL-4 decreased damage volume and number of destroyed neurons. IL-4 stopped TNF-α whereas upregulated TGF-β, IL-10, and Arg1 expressions. Iba1/Arg1 positive macrophage/microglia was notably increased 48 h after IL-4 administration. IL-4 suppresses TBI-induced acceleration of epileptogenesis in rats by directing TBI neuroinflammation toward an anti-inflammatory tone and inhibition of cell death.
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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 Socratic graph.