Cellular infiltration in traumatic brain injury

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.

Possible Link between SARS-CoV-2 Infection and Parkinson’s Disease: The Role of Toll-Like Receptor 4

“…A growing body of evidence indicates that neuroinflammation is involved in the pathogenesis of several neurodegenerative diseases including PD [54][55][56][57], Alzheimer's disease (AD) [58], amyotrophic lateral sclerosis [59], Huntington's disease, and virus-associated dementia [60,61]. Neuroinflammation implicates the recruitment of immune and nonimmune cells at the site of injury or infection, such as resident macrophages, i.e., microglia, aside from astrocytes, endothelial cells, infiltrating T-lymphocytes, α-SYN reactive Tlymphocytes, and major histocompatibility complex (MHC) class II-positive microglia [62][63][64][65]. Microglia are the most abundant populations in the brain parenchyma and represent the major cell type involved in neuroinflammation However, sophisticated neuronmicroglia-astrocyte crosstalk also plays a critical role in the immune response [66][67][68].…”

Immunological Responses to Transgene-Modified Neural Stem Cells After Transplantation

“…Iba-1 positive cells and MHC-II positive cells exhibited similar changes both on day 3 and day 21 after transplantation. MHC-I-positive cells exhibit changes in the brain similar to those seen with brain injury ( 50 ). Considering the above evidence, we speculated that the levels of cytokines and inflammatory factors increased sharply in the early stage of transplantation but decreased as the brain injury recovered.…”

“…We have studied the immune rejection of allogeneic gene-modified stem cell transplantation, but we have not systematically evaluated the immune response at the levels of cytokines and inflammatory factors. Several studies have proved that microglia activation can result in antigen presentation and the secretion of cytokines such as interleukin-1 beta (IL-1β), IFN-γ, and TNF-α ( 46 – 50 ). However, one study found that IFN-γ treatment induced a degree of activation of MHC-II but not MHC-II ( 46 ), while another reported that TNF-α did not impact the numbers of MHC-II immunoreactive cells ( 51 ).…”

Cordycepin confers long-term neuroprotection via inhibiting neutrophil infiltration and neuroinflammation after traumatic brain injury

“…WMI in TBI is escalated by altered microglial/macrophage functional state and subsequent neuroinflammation [ 8 ]. After TBI, peripheral immune cells are recruited into the brain parenchyma and whereby exacerbate the breakdown of the brain-blood barrier (BBB) and promote microglia/macrophages to polarize toward a pro-inflammatory state [ 9 , 10 ]. BBB disruption can simultaneously cause microglial activation in return, forming a feed-forward loop [ 11 , 12 ].…”