Neural Regeneration Research ›› 2019, Vol. 14 ›› Issue (9): 1481-1489.doi: 10.4103/1673-5374.255958

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Acute drivers of neuroinflammation in traumatic brain injury

Kathryn L. Wofford 1, 2, 3 , David J. Loane 4, 5 , D. Kacy Cullen 1, 2, 6   

  1. 1 Center for Brain Injury & Repair, Department of Neurosurgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA
    2 Center for Neurotrauma, Neurodegeneration & Restoration, Corporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, USA
    3 School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA, USA
    4 Department of Anesthesiology and Shock, Trauma, and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, MD, USA
    5 School of Biochemistry and Immunology and Trinity Biomedical Sciences Institute, Trinity College Dublin, Ireland
    6 Department of Bioengineering, School of Engineering and Applied Science, University of Pennsylvania, Philadelphia, PA, USA
  • Online:2019-09-15 Published:2019-09-15
  • Contact: D. Kacy Cullen, PhD, dkacy@pennmedicine.upenn.edu.
  • Supported by:

    The work was supported by the Department of Veterans Affairs, USA (Merit Review I01-RX001097 & I01-BX003748).

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Abstract:

Neuroinflammation is initiated as a result of traumatic brain injury and can exacerbate evolving tissue pathology. Immune cells respond to acute signals from damaged cells, initiate neuroinflammation, and drive the pathological consequences over time. Importantly, the mechanism(s) of injury, the location of the immune cells within the brain, and the animal species all contribute to immune cell behavior following traumatic brain injury. Understanding the signals that initiate neuroinflammation and the context in which they appear may be critical for understanding immune cell contributions to pathology and regeneration. Within this paper, we review a number of factors that could affect immune cell behavior acutely following traumatic brain injury.

Key words: traumatic brain injury, inflammation, neuroinflammation, microglia, macrophage, acute, diffuse brain injury, cytokines, adenosine 5′-triphosphoate, glutamate, calcium