Inflammation and neuroprotection in traumatic brain injury.
Open accessAbstract
IMPORTANCE: Traumatic brain injury (TBI) is a significant public health concern that affects individuals in all demographics. With increasing interest in the medical and public communities, understanding the inflammatory mechanisms that drive the pathologic and consequent cognitive outcomes can inform future research and clinical decisions for patients with TBI. OBJECTIVES: To review known inflammatory mechanisms in TBI and to highlight clinical trials and neuroprotective therapeutic manipulations of pathologic and inflammatory mechanisms of TBI. EVIDENCE REVIEW: We searched articles in PubMed published between 1960 and August 1, 2014, using the following keywords: traumatic brain injury, sterile injury, inflammation, astrocytes, microglia, monocytes, macrophages, neutrophils, T cells, reactive oxygen species, alarmins, danger-associated molecular patterns, purinergic receptors, neuroprotection, and clinical trials. Previous clinical trials or therapeutic studies that involved manipulation of the discussed mechanisms were considered for inclusion. The final list of selected studies was assembled based on novelty and direct relevance to the primary focus of this review. FINDINGS: Traumatic brain injury is a diverse group of sterile injuries induced by primary and secondary mechanisms that give rise to cell death, inflammation, and neurologic dysfunction in patients of all demographics. Pathogenesis is driven by complex, interacting mechanisms that include reactive oxygen species, ion channel and gap junction signaling, purinergic receptor signaling, excitotoxic neurotransmitter signaling, perturbations in calcium homeostasis, and damage-associated molecular pattern molecules, among others. Central nervous system resident and peripherally derived inflammatory cells respond to TBI and can provide neuroprotection or participate in maladaptive secondary injury reactions. The exact contribution of inflammatory cells to a TBI lesion is dictated by their anatomical positioning as well as the local cues to which they are exposed. CONCLUSIONS AND RELEVANCE: The mechanisms that drive TBI lesion development as well as those that promote repair are exceedingly complex and often superimposed. Because pathogenic mechanisms can diversify over time or even differ based on the injury type, it is important that neuroprotective therapeutics be developed and administered with these variables in mind. Due to its complexity, TBI has proven particularly challenging to treat; however, a number of promising therapeutic approaches are now under pre-clinical development, and recent clinical trials have even yielded a few successes. Given the worldwide impact of TBI on the human population, it is imperative that research remains active in this area and that we continue to develop therapeutics to improve outcome in afflicted patients.
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Meningeal immune cells play an important role in the brain injury response.
“numerous studies show that meningeal immune cells play an important role in the brain injury response”
From Living on the Edge of the CNS: Meninges Cell Diversity in Health and Disease (2021) · cites this paper as Corps et al., 2015
HMGB1 has a pivotal role in the induction of neuroinflammatory processes in neurodegenerative conditions, cerebral ischemia, traumatic brain injury, seizure, and ethanol-induced neurotoxicity.
“HMGB1 has a pivotal role in the induction of neuroinflammatory processes in neurodegenerative conditions (Fang et al, 2012), cerebral ischemia (Yang et al, 2010), traumatic brain injury (Corps et al, 2015), seizure (Vezzani, 2014), and ethanolinduced neurotoxicity (Zou and Crews, 2014).”
From Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders (2017) · cites this paper as Corps et al, 2015
Purinergic receptors play an important role in TBI by detecting ATP and uridine 5′-diphosphate, which are released after tissue damage.
“Purinergic receptors also play an important role in TBI by detecting adenosine 5′-triphosphate (ATP) and uridine 5′-diphosphate, which are released after tissue damage (133).”
From The anatomy and immunology of vasculature in the central nervous system (2019) · cites this paper as [133]
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- Authors
- Corps, K. N., Roth, T. L., & McGavern, D. B.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- McGavern, Dorian B.
- Venue
- JAMA Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2015-03-01
- Volume
- 72
- Issue
- 3
- Pages
- 355
- ISSN
- 2168-6149 (ISSN-L)
- PMC
- PMC5001842
- OpenAlex
- W2137368645
- Cited by
- 853
- References
- 64
- Citations by year
- 2026: 56 · 2025: 91 · 2024: 83 · 2023: 78 · 2022: 99 · 2021: 91 · 2020: 91 · 2019: 75 · 2018: 57 · 2017: 54 · 2016: 50 · 2015: 26
- FWCI
- 43.95
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- JAMA Neurology (publishedVersion)
- PubMed (publishedVersion)
- 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
- traumatic brain injury, neuroinflammation, neuroprotection, sterile inflammation, reactive oxygen species, damage-associated molecular patterns, purinergic receptors, astrocytes, microglia, macrophages, neutrophils, T cells, excitotoxicity, calcium homeostasis, gap junction signaling, ion channels, alarmins, secondary injury
- MeSH terms
- Animals, Brain Injuries, Clinical Trials as Topic, Humans, Inflammation, Reactive Oxygen Species, Neuroprotective Agents
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