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Review
. 2023 Jun 23;102(25):e34009.
doi: 10.1097/MD.0000000000034009.

Research progress of neuroinflammation-related cells in traumatic brain injury: A review

Affiliations
Review

Research progress of neuroinflammation-related cells in traumatic brain injury: A review

Qinghui Zhao et al. Medicine (Baltimore). .

Abstract

Neuroinflammation after traumatic brain injury (TBI) is related to chronic neurodegenerative diseases and is one of the causes of acute secondary injury after TBI. Therefore, it is particularly important to clarify the role of cellular mechanisms in the neuroinflammatory response after TBI. The objective of this article is to understand the involvement of cells during the TBI inflammatory response (for instance, astrocytes, microglia, and oligodendrocytes) and shed light on the recent progress in the stimulation and interaction of granulocytes and lymphocytes, to provide a novel approach for clinical research. We searched articles in PubMed published between 1950 and 2023, using the following keywords: TBI, neuroinflammation, inflammatory cells, neuroprotection, clinical. Articles for inclusion in this paper were finalized based on their novelty, representativeness, and relevance to the main arguments of this review. We found that the neuroinflammatory response after TBI includes the activation of glial cells, the release of inflammatory mediators in the brain, and the recruitment of peripheral immune cells. These inflammatory responses not only induce secondary brain damage, but also have a role in repairing the nervous system to some extent. However, not all of the mechanisms of cell-to-cell interactions have been well studied. After TBI, clinical treatment cannot simply suppress the inflammatory response, and the inflammatory phenotype of patients' needs to be defined according to their specific conditions after injury. Clinical trials of personalized inflammation regulation therapy for specific patients should be carried out in order to improve the prognosis of patients.

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Conflict of interest statement

The authors have no conflicts of interest to disclose.

Figures

Figure 1.
Figure 1.
Inflammatory response and microglia initiation after TBI. TBI = traumatic brain injury.
Figure 2.
Figure 2.
Inflammatory response and astrocyte initiation after TBI. TBI = traumatic brain injury.
Figure 3.
Figure 3.
Inflammatory response and oligodendrocyte initiation after TBI. TBI = traumatic brain injury.

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References

    1. Ruff RL, Riechers RG. Effective treatment of traumatic brain injury: learning from experience. JAMA. 2012;308:2032–3. - PubMed
    1. Taylor CA, Bell JM, Breiding MJ, et al. . Traumatic brain injury-related emergency department visits, hospitalizations, and deaths-United States, 2007 and 2013. MMWR Surveill Summ. 2017;66:1–16. - PMC - PubMed
    1. Jiang JY, Gao GY, Feng JF, et al. . Traumatic brain injury in Chinas. Lancet Neurol. 2019;18:286–95. - PubMed
    1. Maas AIR, Menon DK, Manley GT, et al. .; InTBIR Participants and Investigators. Traumatic brain injury: progress and challenges in prevention, clinical care, and research. Lancet Neurol. 2022;21:1004–60. - PMC - PubMed
    1. Hicks AJ, Ponsford JL, Spitz G, et al. . β-Amyloid and Tau imaging in chronic traumatic brain injury: a cross-sectional study. Neurology. 2022;99:e1131–41. - PubMed