Dynamic change in cortisol levels associated with severity, progression, and survival of patients with traumatic brain injury

Traumatic brain injury (TBI) can cause major disability and increases the risk of neurodegeneration. Post-TBI, there is infiltration of peripheral myeloid and lymphoid cells; there is limited information on the peripheral immune response post-TBI in the immature brain—where injury may interfere with neurodevelopment. We carried out two injury types in juvenile mice: invasive TBI with a controlled cortical impact (CCI) and repetitive mild TBI (rmTBI) using weight drop injury and analysed the response at 5- and 35-days post-injury. In the two models, we detected the brain infiltration of immune cells (e.g., neutrophils, monocytes, dendritic cells, CD4+ T cells, and NK cells). There were increases in macrophages, neutrophils, and dendritic cells in the spleen, increases in dendritic cells in blood, and increases in CD8+ T cells and B cells in lymph nodes. These results indicate a complex peripheral immune response post-TBI in the immature brain, with differences between an invasive injury and a repetitive mild injury.

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Dynamic change in cortisol levels associated with severity, progression, and survival of patients with traumatic brain injury

Cited by 4 publications

References 19 publications

Psychedelics for acquired brain injury: a review of molecular mechanisms and therapeutic potential

Psychedelics for acquired brain injury: a review of molecular mechanisms and therapeutic potential

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The Immune Response in Two Models of Traumatic Injury of the Immature Brain

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