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Cellular infiltration in traumatic brain injury.
Alam, Aftab; Thelin, Eric P; Tajsic, Tamara; Khan, Danyal Z; Khellaf, Abdelhakim; Patani, Rickie; Helmy, Adel.
Afiliación
  • Alam A; Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK. alam.camb@gmail.com.
  • Thelin EP; Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
  • Tajsic T; Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
  • Khan DZ; Department of Neurology, Karolinska University Hospital, Stockholm, Sweden.
  • Khellaf A; Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
  • Patani R; Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
  • Helmy A; Division of Neurosurgery, Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
J Neuroinflammation ; 17(1): 328, 2020 Nov 03.
Article en En | MEDLINE | ID: mdl-33143727
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.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Encéfalo / Astrocitos / Microglía / Lesiones Traumáticas del Encéfalo / Neuronas Límite: Animals / Humans Idioma: En Revista: J Neuroinflammation Asunto de la revista: NEUROLOGIA Año: 2020 Tipo del documento: Article País de afiliación: Reino Unido

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Encéfalo / Astrocitos / Microglía / Lesiones Traumáticas del Encéfalo / Neuronas Límite: Animals / Humans Idioma: En Revista: J Neuroinflammation Asunto de la revista: NEUROLOGIA Año: 2020 Tipo del documento: Article País de afiliación: Reino Unido