ArticleInternational journal of molecular sciences2020
Antagonism of Macrophage Migration Inhibitory Factory (MIF) after Traumatic Brain Injury Ameliorates Astrocytosis and Peripheral Lymphocyte Activation and Expansion.
Article in International journal of molecular sciences, 2020. 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, 23 citations in OpenAlex.
- Photobiomodulation restores blood-brain barrier integrity after hypoxia via endothelial von Willebrand factor modulation in a humanised tricellular transwell model.The Journal of physiology · 2026Article
- CD44 antagonism after traumatic brain injury influences the adult neurogenic niche and behavioral outcomes.Brain structure & function · 2026Article
- Sex differences in neurobehavior and the adult hippocampal neurogenic niche: influence of traumatic brain injury and CLIP antagonism.Frontiers in behavioral neuroscience · 2026Article
- MIF downregulation attenuates neuroinflammation via TLR4/MyD88/TRAF6/NF-κB pathway to protect dopaminergic neurons in Parkinson's disease model.Communications biology · 2025Article
- Traumatic brain injury exacerbates alcohol consumption and neuroinflammation with decline in cognition and cholinergic activity.Translational psychiatry · 2025Article
- Glial Activation Enhances Spinal TRPV1 Receptor Sensitivity in a Paclitaxel Model of Neuropathic Pain.Physiological research · 2025Article
- Traumatic brain injury alters the effects of class II invariant peptide (CLIP) antagonism on chronic meningeal CLIP + B cells, neuropathology, and neurobehavioral impairment in 5xFAD mice.Journal of neuroinflammation · 2024Article
- Sex-Specific and Traumatic Brain Injury Effects on Dopamine Receptor Expression in the Hippocampus.International journal of molecular sciences · 2023Article
- Dualistic roles and mechanistic insights of macrophage migration inhibitory factor in brain injury and neurodegenerative diseases.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Stem Cell Therapy for Sequestration of Traumatic Brain Injury-Induced Inflammation.International journal of molecular sciences · 2022Review
- Unilateral Cervical Vagotomy Modulates Immune Cell Profiles and the Response to a Traumatic Brain Injury.International journal of molecular sciences · 2022Article
- Revisiting Excitotoxicity in Traumatic Brain Injury: From Bench to Bedside.Pharmaceutics · 2022Review
- MIF promotes neurodegeneration and cell death via its nuclease activity following traumatic brain injury.Cellular and molecular life sciences : CMLS · 2021Article
- Credibility of the Neutrophil-to-Lymphocyte Count Ratio in Severe Traumatic Brain Injury.Life (Basel, Switzerland) · 2021Review
- Review
- Neuropathophysiological Mechanisms and Treatment Strategies for Post-traumatic Epilepsy.Frontiers in molecular neuroscience · 2021Review
- Vagus Nerve Stimulation Ameliorates Cognitive Impairment and Increased Hippocampal Astrocytes in a Mouse Model of Gulf War Illness.Neuroscience insights · 2021Article
- γδ T Cells Participating in Nervous Systems: A Story of Jekyll and Hyde.Frontiers in immunology · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) precedes the onset of epilepsy in up to 15-20% of symptomatic epilepsies and up to 5% of all epilepsy. Treatment of acquired epilepsies, including post-traumatic epilepsy (PTE), presents clinical challenges, including frequent resistance to anti-epileptic therapies. Considering that over 1.6 million Americans present with a TBI each year, PTE is an urgent clinical problem. Neuroinflammation is thought to play a major causative role in many of the post-traumatic syndromes, including PTE. Increasing evidence suggests that neuroinflammation facilitates and potentially contributes to seizure induction and propagation. The inflammatory cytokine, macrophage migration inhibitory factor (MIF), is elevated after TBI and higher levels of MIF correlate with worse post-traumatic outcomes. MIF was recently demonstrated to directly alter the firing dynamics of CA1 pyramidal neurons in the hippocampus, a structure critically involved in many types of seizures. We hypothesized that antagonizing MIF after TBI would be anti-inflammatory, anti-neuroinflammatory and neuroprotective. The results show that administering the MIF antagonist ISO1 at 30 min after TBI prevented astrocytosis but was not neuroprotective in the peri-lesion cortex. The results also show that ISO1 inhibited the TBI-induced increase in γδT cells in the gut, and the percent of B cells infiltrating into the brain. The ISO1 treatment also increased this population of B cells in the spleen. These findings are discussed with an eye towards their therapeutic potential for post-traumatic syndromes, including PTE.
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