Cited by 149Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchNeuroinflammation and Neurodegeneration Mechanisms

Distinct myeloid cell subsets promote meningeal remodeling and vascular repair after mild traumatic brain injury

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Russo, Matthew V., Latour, Lawrence L., McGavern, Dorian B.·2018·Nature Immunology

Abstract

Mild traumatic brain injury (mTBI) can cause meningeal vascular injury and cell death that spreads into the brain parenchyma and triggers local inflammation and recruitment of peripheral immune cells. The factors that dictate meningeal recovery after mTBI are unknown at present. Here we demonstrated that most patients who had experienced mTBI resolved meningeal vascular damage within 2-3 weeks, although injury persisted for months in a subset of patients. To understand the recovery process, we studied a mouse model of mTBI and found extensive meningeal remodeling that was temporally reliant on infiltrating myeloid cells with divergent functions. Inflammatory myelomonocytic cells scavenged dead cells in the lesion core, whereas wound-healing macrophages proliferated along the lesion perimeter and promoted angiogenesis through the clearance of fibrin and production of the matrix metalloproteinase MMP-2. Notably, a secondary injury experienced during the acute inflammatory phase aborted this repair program and enhanced inflammation, but a secondary injury experienced during the wound-healing phase did not. Our findings demonstrate that meningeal vasculature can undergo regeneration after mTBI that is dependent on distinct myeloid cell subsets.

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  • Vascular repair was observed in the meninges after TBI and was dependent on the recruitment of nonclassical monocytes from the blood.

    “Vascular repair was also observed in the meninges after TBI and was dependent on the recruitment of nonclassical monocytes from the blood (127).”
  • TBI can disrupt vascular integrity in the meninges and brain parenchyma, resulting in leakage of materials from the blood supply into CNS.

    “TBI can disrupt vascular integrity in the meninges and brain parenchyma, resulting in leakage of materials from the blood supply into CNS (Fig. 4) (125-127).”

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Authors
Russo, M. V., Latour, L. L., & McGavern, D. B.
Affiliations
National Institutes of Health (US)
Corresponding author
McGavern, Dorian B.
Venue
Nature Immunology
Published
2018-04-16
Volume
19
Issue
5
Pages
442-452
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
OpenAlex
W2802914527
Cited by
149
References
59
Citations by year
2026: 7 · 2025: 23 · 2024: 23 · 2023: 17 · 2022: 26 · 2021: 25 · 2020: 8 · 2019: 13 · 2018: 7
FWCI
8.93
Type
journal article
Language
en
Open access
Locations
  • Nature Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute of Neurological Disorders and Stroke (ZIANS003112)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
mild traumatic brain injury, myeloid cells, myelomonocytes, angiogenesis, fibrin clearance, MMP-2, secondary injury, meningeal inflammation
MeSH terms
Animals, Blood-Brain Barrier, Brain Concussion, Female, Humans, Male, Meninges, Neovascularization, Physiologic, Myeloid Cells, Mice

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