Cellular infiltration in traumatic brain injury.


Type
Article
Change log
Authors
Thelin, Eric P 
Tajsic, Tamara 
Khan, Danyal Z 
Khellaf, Abdelhakim 
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.

Description
Keywords
Cellular infiltration, Microglial dynamics, Neuroinflammation, Traumatic brain injury, Animals, Astrocytes, Brain, Brain Injuries, Traumatic, Chemokines, Cytokines, Encephalitis, Humans, Microglia, Neurons
Journal Title
J Neuroinflammation
Conference Name
Journal ISSN
1742-2094
1742-2094
Volume Title
17
Publisher
Springer Science and Business Media LLC
Rights
All rights reserved
Sponsorship
Medical Research Council (G0802251)
Royal College of Surgeons of England (2016/2017)
Medical Research Council (MR/R005036/1)
Academy of Medical Sciences (Unknown)
This work has been supported by the Medical Research Council, UK (MR/R005036/1). AA is supported as Newton International Fellow by the Academy of Medical Sciences and Newton Fund, UK (NF170920). AH is supported by the NIHR Biomedical Research Campus and The Royal College of Surgeons of England. EPT is supported by grants from Svenska Sällskapet för Medicinsk Forskning (SSMF), Hjärnfonden and Region Stockholm ALF. RP holds an MRC Senior Clinical Fellowship [MR/S006591/ 1].