Brain and microglia gene expression 30 days after traumatic brain injury and post-injury sleep fragmentation
Traumatic brain injury (TBI) is a global source of injury-related death and disability, and survivors often suffer functional and psychiatric consequences that persist for years. Neuroinflammation, mediated in part by microglia, perpetuates chronic dysfunction after TBI and leaves survivors vulnerable to the effects of secondary immune challenges. Previous data from our lab shows that 30 days of mechanical sleep fragmentation (SF) aggravates microglia-associated neuroinflammation in C57BL/6 mice, impairing recovery after TBI. To better understand the mechanisms through which microglia contribute to impairment following post-TBI SF, we used bulk RNA sequencing to analyze gene expression in microglia and coronal slice from the ipsilateral brain of C57BL/6 mice who received a TBI or sham injury followed by 30 days of SF or control housing. We analyzed differentially expressed genes (DEGs) within each tissue type to determine how ipsilateral brain and microglia are independently influenced by TBI and SF. We also compared microglial DEGS directly to those of coronal slice, gaining novel insight into how microglia contribute to dysfunction in the ipsilateral brain after TBI and post-injury SF.