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A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
Published on: June 10, 2020
Priming the inflammatory pump of the CNS after traumatic brain injury
Kristina G Witcher1, Daniel S Eiferman2, Jonathan P Godbout3
1Department of Neuroscience, The Ohio State University, 333 West 10th Avenue, Columbus, OH, USA.
Abstract:
Traumatic brain injury (TBI) can lead to secondary neuropsychiatric problems that develop and persist years after injury. Mounting evidence indicates that neuroinflammatory processes progress after the initial head injury and worsen with time. Microglia contribute to this inflammation by maintaining a primed profile long after the acute effects of the injury have dissipated. This may set the stage for glial dysfunction and hyperactivity to challenges including subsequent head injury, stress, or induction of a peripheral immune response. This review discusses the evidence that microglia become primed following TBI and how this corresponds with vulnerability to a 'second hit' and subsequent neuropsychiatric and neurodegenerative complications.
Insights
Traumatic brain injury (TBI) primes microglia, increasing long-term vulnerability to neuroinflammation and subsequent neuropsychiatric or neurodegenerative issues. This priming effect highlights a critical window for secondary complications after the initial injury.
Area of Science:
- Neuroscience
- Immunology
- Neurology
Background:
- Traumatic brain injury (TBI) can trigger long-term neuroinflammatory responses.
- Microglia, the brain's immune cells, remain activated long after the initial injury.
- This sustained microglial activation is linked to secondary neuropsychiatric and neurodegenerative conditions.
Purpose of the Study:
- To review the evidence for microglial priming following TBI.
- To explore the link between microglial priming and heightened vulnerability to secondary insults.
- To discuss the implications for neuropsychiatric and neurodegenerative complications.
Main Methods:
- Literature review of studies investigating TBI, neuroinflammation, and microglial activation.
- Synthesis of evidence on the temporal dynamics of microglial responses post-TBI.
- Analysis of the 'second hit' hypothesis in the context of TBI.
Main Results:
- Evidence suggests microglia adopt a primed state after TBI, persisting long-term.
- This primed state enhances microglial reactivity to subsequent challenges.
- Primed microglia contribute to ongoing neuroinflammation and glial dysfunction.
Conclusions:
- Microglial priming is a key mechanism linking TBI to chronic neuroinflammation.
- TBI-induced microglial priming increases susceptibility to neuropsychiatric and neurodegenerative diseases.
- Understanding microglial priming is crucial for developing interventions for TBI complications.
