Abstract
Although, there is growing awareness in the progressive neurodegeneration of chronic traumatic encephalopathy, changes of immune reactions remain equivocal at best. Thus, in a clinically relevant rat repetitive mild traumatic brain injury (rmTBI) model, some immunologic cells (T cell subsets, microglia) in the injured brain and peripheral blood were analyzed by flow cytometry and immunofluorescence. In the injured brain, CD3+ T cells showed a bimodal increase during 42 days post-injury (dpi). CD3+CD4+ T cells firstly increased and then decreased, while CD3+CD8+ T cells had reversed tendency. CD86+/CD11b+ M1-like microglia increased at 42 dpi and CD206+/CD11b+ M2-like microglia peaked at 7 dpi. In addition, peripheral immune suppression was implicated in the chronic phase after rmTBI. Taken together, the study provided useful information on long-term dynamic changes of some immune cells after rmTBI in rats.
Highlights
Traumatic brain injury (TBI) is a major public health issue, which caused by road traffic collisions, assaults, and falls, etc
T lymphocyte subsets were characterized by the expression of cell surface markers: all T cells (CD3+), CD4+ or C D8+ T cells (CD3+CD4+ or CD3+CD8+) [2]
The percentage of C D8+ T cells decreased during 7 dpi, and returned to the baseline level at 42 dpi (Fig. 2b)
Summary
Traumatic brain injury (TBI) is a major public health issue, which caused by road traffic collisions, assaults, and falls, etc. Before retired athletes and veterans of wars, chronic traumatic encephalopathy (CTE), a progressive neurodegeneration of the brain tissue or a result of repetitive mild traumatic brain injury (rmTBI) [1], was not considered to be a common phenomenon. TBI elicits robust immune events that leads to axonal damage and secondary injury. Changes of T cell subsets and microglia post-rmTBI remain incomplete.
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