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The Duality of the Inflammatory Response to Traumatic Brain Injury
Abstract
One and a half to two million people sustain a traumatic brain injury (TBI) in the US each year, of which approx 70,000-90,000 will suffer from long-term disability with dramatic impacts on their own and their families' lives and enormous socio-economic costs. Brain damage following traumatic injury is a result of direct (immediate mechanical disruption of brain tissue, or primary injury) and indirect (secondary or delayed) mechanisms. These secondary mechanisms involve the initiation of an acute inflammatory response, including breakdown of the blood-brain barrier (BBB), edema formation and swelling, infiltration of peripheral blood cells and activation of resident immunocompetent cells, as well as the intrathecal release of numerous immune mediators such as interleukins and chemotactic factors. An overview over the inflammatory response to trauma as observed in clinical and in experimental TBI is presented in this review. The possibly harmful/beneficial sequelae of post-traumatic inflammation in the central nervous system (CNS) are discussed using three model mediators of inflammation in the brain, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and transforming growth factor-beta (TGF-beta). While the former two may act as important mediators for the initiation and the support of post-traumatic inflammation, thus causing additional cell death and neurologic dysfunction, they may also pave the way for reparative processes. TGF-beta, on the other hand, is a po…
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These mechanisms range from inflammatory and glutamate excitotoxicity pathways, which increase metabolic demands of neurons and microglia, to oxidative stress pathways that may impact mitochondrial function.
“They range from inflammatory and glutamate excitotoxicity pathways (57;58), which increase the metabolic demands of neurons and microglia, to oxidative stress pathways that may impact mitochondrial function (59).”
From Association of ALS with head injury, cigarette smoking and APOE genotypes (2010) · cites this paper as [57]
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Metadata
- Authors
- McIntosh, T. K., Lenzlinger, P. M., Morganti-Kossmann, M.-C., & Laurer, H. L.
- Affiliations
- University of Pennsylvania (US)
- Philadelphia VA Medical Center (US)
- University Hospital Zurich (CH)
- Corresponding author
- McIntosh, Tracy K.
- Venue
- Molecular Neurobiology
- Published
- 2001
- Volume
- 24
- Issue
- 1-3
- Pages
- 169-182
- ISSN
- 0893-7648 (ISSN-L)
- OpenAlex
- W2067487401
- Cited by
- 428
- References
- 7
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 8 · 2023: 6 · 2022: 7 · 2021: 13 · 2020: 11 · 2019: 13 · 2018: 15 · 2017: 21 · 2016: 24 · 2015: 24 · 2014: 30 · 2013: 36 · 2012: 42
- FWCI
- 6.72
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM034690)
- National Institute of Neurological Disorders and Stroke (P50NS008803, R01NS040978, T32 NS07413-04, T32NS007413)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- traumatic brain injury, post-traumatic inflammation, secondary injury mechanisms, blood-brain barrier disruption, cerebral edema, neuroinflammation, TNF-α, interleukin-6, TGF-beta, anti-inflammatory therapy, neuroprotection, central nervous system
- MeSH terms
- Animals, Brain Injuries, Humans, Inflammation, Models, Biological, Cytokines
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