Authors:

Abby Wertz

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About Paper:

Traumatic Brain Injury (TBI) accounts for approximately one-third of injury-related deaths in the United States. In aged mice, microglia facilitate recruitment of CD8+ T cells to the brain following TBI, contributing to worsened health outcomes, including decreased motor and cognitive abilities. Microglia depletion in aged mice reduces CD8+ T cell infiltration. Since CD8+ T cell infiltration is not typically observed in young mice, we hypothesized that microglia depletion would not affect this recruitment post-injury. Young male and female mice (12 weeks, n=5/group) underwent microglia depletion via a PLX5622, a colony-stimulating factor 1 receptor inhibitor, diet, or were placed on a control diet. Mice underwent TBI using controlled cortical impact or sham injury, in which an incision was made, but TBI was not induced. Eight hours post-injury, mice were euthanized, and brain and blood samples were collected. Flow cytometry confirmed microglia depletion in the PLX5622 diet group and quantified leukocyte and CD8+ T cell populations. Microglia depletion in young male mice did not result in significant differences in T cell populations 8 hours post-TBI compared to the control diet groups (p > 0.05). No significant differences were observed between CD8+ T cell or leukocyte populations in the microglia depletion groups compared to control diet groups or between the TBI and sham injury groups 8 hours post-injury (p > 0.05). These findings support our hypothesis that microglia depletion does not influence CD8+ T cell infiltration in the young mouse brain at 8 hours post-injury. Additionally, these results suggest that CD8+ T cell infiltration after TBI is an age-dependent mechanism. Understanding the interactions between microglia and CD8+ T cell recruitment is crucial for confirming that CD8+ T cell infiltration is age-specific, which may reflect similar mechanisms in humans.

Source:

Northwestern University

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Co-authors:

Abby Wertz