Cellular infiltration in traumatic brain injury.
Aftab AlamEric P ThelinTamara TajsicDanyal Z KhanAbdelhakim KhellafRickie PataniAdel HelmyPublished in: Journal of neuroinflammation (2020)
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.
Keyphrases
- traumatic brain injury
- brain injury
- oxidative stress
- cerebral ischemia
- resting state
- white matter
- subarachnoid hemorrhage
- induced apoptosis
- dendritic cells
- inflammatory response
- spinal cord
- functional connectivity
- peripheral blood
- fluorescent probe
- neuropathic pain
- blood brain barrier
- sensitive detection
- cell proliferation
- patient safety
- cross sectional
- immune response
- quality improvement
- high intensity
- multiple sclerosis
- single molecule
- cerebrospinal fluid
- cell death
- cell cycle arrest
- loop mediated isothermal amplification