Cellular infiltration in traumatic brain injury
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Cellular infiltration in traumatic brain injury Aftab Alam1* , Eric P. Thelin1,2,3, Tamara Tajsic1, Danyal Z. Khan1, Abdelhakim Khellaf1,4, Rickie Patani5,6 and Adel Helmy1
Abstract Traumatic brain injury leads to cellular damage which in turn results in the rapid release of damage-associated molecular patterns (DAMPs) that prompt resident cells to release cytokines and chemokines. These in turn rapidly recruit neutrophils, which assist in limiting the spread of injury and removing cellular debris. Microglia continuously survey the CNS (central nervous system) compartment and identify structural abnormalities in neurons contributing to the response. After some days, when neutrophil numbers start to decline, activated microglia and astrocytes assemble at the injury site—segregating injured tissue from healthy tissue and facilitating restorative processes. Monocytes infiltrate the injury site to produce chemokines that recruit astrocytes which successively extend their processes towards monocytes during the recovery phase. In this fashion, monocytes infiltration serves to help repair the injured brain. Neurons and astrocytes also moderate brain inflammation via downregulation of cytotoxic inflammation. Depending on the severity of the brain injury, T and B cells can also be recruited to the brain pathology sites at later time points. Keywords: Neuroinflammation, Cellular infiltration, Traumatic brain injury, Microglial dynamics
Background Traumatic brain injury (TBI) results from force transmission to the head either by impact with an object or from acceleration/deceleration forces that produce vigorous movement of the brain within the skull or varying combinations of these mechanical forces [1]. It is now widely acknowledged that TBI is a multimodal complex disease process and not a single pathophysiological event [2]. It triggers structural and functional changes leading to neuronal injury which can be classified into primary and secondary brain injury [3]. Primary injury is caused by external forces (direct contact and/ or inertial forces to the brain) acting at the moment of the injury that damages the blood vessels, axons, nerve cells, and glia of the brain in a focal, multifocal, or diffuse pattern of involvement. The type and severity of the resulting injury depends upon the nature of the original force plus the site, direction, and magnitude of the force [4]. In contrast, secondary injury is an ongoing process that occurs from * Correspondence: [email protected] 1 Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK Full list of author information is available at the end of the article
minutes to years following the initial insult. Secondary injury is the result of the cascades of metabolic, neurochemical, cellular and molecular events stemming from primary insult [5]. Such mechanisms ultimately lead to brain cell death, plasticity, tissue damage and atrophy [6–8]. Some of the biochemical alterations responsible for secondary injury a
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