ReviewFrontiers in immunology2021
Inflammatory Regulation of CNS Barriers After Traumatic Brain Injury: A Tale Directed by Interleukin-1.
Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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Who cites it
36 citing papers in PubMed.
- Peripheral macrophages and T-cells accumulate in the degenerating optic tract after repetitive head impact.Brain, behavior, and immunity · 2026Article
- Repeated head impacts establish a senescent cranial bone marrow niche that impairs brain metabolism.Journal of neuroinflammation · 2026Article
- Primary Blast-Induced Traumatic Brain Injury as a Risk Factor for (Cerebro)vascular Disorder: Clinical Manifestations, Blast Physics, Biomechanics, Pathobiology, and Critical Gaps.International journal of molecular sciences · 2026Review
- Integrative Peptide Drug Development: Chemical Engineering, AI-Driven Design, and Cell-Penetrating Peptides.Pharmaceutics · 2026Review
- Repeated Mild Head Injury Establishes a Senescent Cranial Bone Marrow Niche that Impairs Brain Metabolism.bioRxiv : the preprint server for biology · 2026Article
- Uncovering the Role of Thrombospodin-1 and Occludin as Potential Prognostic and Diagnostic Biomarkers in Traumatic Brain Injury.International journal of molecular sciences · 2026Article
- Cytokines and related signaling pathways in traumatic brain injury.Frontiers in immunology · 2026Review
- Multifunctional Nanoparticles in Traumatic Brain Injury: From Targeted Imaging and Diagnosis to Innovative Therapeutics.International journal of nanomedicine · 2026Review
- Temporal Evolution of Brain Inflammation in the Bilateral Common Carotid Artery Stenosis Model of Chronic Cerebral Hypoperfusion.Journal of inflammation research · 2026Review
- 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
- Three-Dimensional Human Neurovascular Unit Modeling Reveals Cell-Specific Mechanisms of Traumatic Brain Injury.Journal of functional biomaterials · 2025Article
- Perceiving traumatic brain injury from glymphatic system.Molecular psychiatry · 2025Review
- Serum IL-6, IL-1b, IL-8, and cerebrospinal fluid biochemical profiles in patients with lateral skull base temporal bone fractures and cerebrospinal fluid leak.Journal of medical biochemistry · 2025Article
- The Relationship Between Inflammation and the Development of Cerebral Ischaemia and Hypoxia in Traumatic Brain Injury-A Narrative Review.International journal of molecular sciences · 2025Review
- Advances in ERK Signaling Pathway in Traumatic Brain Injury: Mechanisms and Therapeutic Potential.Neurochemical research · 2025Review
- Review
- Eyes Are the Windows to the Soul: Reviewing the Possible Use of the Retina to Indicate Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- Single cell RNA sequencing after moderate traumatic brain injury: effects of therapeutic hypothermia.Journal of neuroinflammation · 2025Article
- The Crucial Role of the Blood-Brain Barrier in Neurodegenerative Diseases: Mechanisms of Disruption and Therapeutic Implications.Journal of clinical medicine · 2025Review
- Choroid Plexus Pathophysiology.Annual review of pathology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Several barriers separate the central nervous system (CNS) from the rest of the body. These barriers are essential for regulating the movement of fluid, ions, molecules, and immune cells into and out of the brain parenchyma. Each CNS barrier is unique and highly dynamic. Endothelial cells, epithelial cells, pericytes, astrocytes, and other cellular constituents each have intricate functions that are essential to sustain the brain's health. Along with damaging neurons, a traumatic brain injury (TBI) also directly insults the CNS barrier-forming cells. Disruption to the barriers first occurs by physical damage to the cells, called the primary injury. Subsequently, during the secondary injury cascade, a further array of molecular and biochemical changes occurs at the barriers. These changes are focused on rebuilding and remodeling, as well as movement of immune cells and waste into and out of the brain. Secondary injury cascades further damage the CNS barriers. Inflammation is central to healthy remodeling of CNS barriers. However, inflammation, as a secondary pathology, also plays a role in the chronic disruption of the barriers' functions after TBI. The goal of this paper is to review the different barriers of the brain, including (1) the blood-brain barrier, (2) the blood-cerebrospinal fluid barrier, (3) the meningeal barrier, (4) the blood-retina barrier, and (5) the brain-lesion border. We then detail the changes at these barriers due to both primary and secondary injury following TBI and indicate areas open for future research and discoveries. Finally, we describe the unique function of the pro-inflammatory cytokine interleukin-1 as a central actor in the inflammatory regulation of CNS barrier function and dysfunction after a TBI.
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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.