Cellular infiltration in traumatic brain injury.
Cellular infiltration
Microglial dynamics
Neuroinflammation
Traumatic brain injury
Journal
Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974
Informations de publication
Date de publication:
03 Nov 2020
03 Nov 2020
Historique:
received:
10
09
2020
accepted:
21
10
2020
entrez:
4
11
2020
pubmed:
5
11
2020
medline:
18
9
2021
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 33143727
doi: 10.1186/s12974-020-02005-x
pii: 10.1186/s12974-020-02005-x
pmc: PMC7640704
doi:
Substances chimiques
Chemokines
0
Cytokines
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
328Subventions
Organisme : Medical Research Council
ID : G0802251
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/R005036/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/S006591/1
Pays : United Kingdom
Organisme : Newton Fund
ID : NF170920
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