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A Novel In Vitro Model of Blast Traumatic Brain Injury
Published on: December 21, 2018
Acute drivers of neuroinflammation in traumatic brain injury
Kathryn L Wofford1, David J Loane2, D Kacy Cullen3
1Center for Brain Injury & Repair, Department of Neurosurgery, Perelman School of Medicine, University of Pennsylvania; Center for Neurotrauma, Neurodegeneration & Restoration, Corporal Michael J. Crescenz Veterans Affairs Medical Center; School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA, USA.
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.
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