Peripheral and central markers of inflammation after experimental brain injury in mice with depleted or intact microglia

  • Rachel K. Rowe (Creator)
  • Katherine R. Giordano (Creator)
  • Maha Saber (Creator)
  • Tabitha R.F. Green (Creator)
  • Luisa M. Rojas-Valencia (Creator)
  • Sean M. Murphy (Creator)
  • Jonathan Lifshitz (Creator)



STUDY PURPOSE: Inflammation is a hallmark of traumatic brain injury (TBI) pathophysiology that contributes to both brain damage and its repair. To investigate microglial mechanisms in central and peripheral inflammation following TBI, we inhibited the colony stimulating factor-1 receptor (CSF-1R), critical for microglial survival, with PLX5622 (PLX). We hypothesized that microglia depletion would attenuate central inflammation acutely. DATA COLLECTED: After randomization, adult male C57BL/6J mice (n = 105) were fed PLX5622 (1200 mg/kg, Plexxikon) or control (AIN-76A rodent chow) diets (21 days) and then received midline fluid percussion injury (mFPI) or sham injury. Blood and brain were collected at 1, 3, or 7 days post-injury (DPI). Immune cell populations (leukocytes, myeloid cells, microglia, monocytes, macrophages, neutrophils) were quantified in the brain and blood by flow cytometry. Pro-inflammatory cytokines (interleukin [IL]-6, IL-1?, tumor necrosis factor [TNF]-?, IFN [interferon]-?) and anti-inflammatory cytokines (IL-10, IL-17A) were quantified in the blood using multiplex ELISA. DATA USAGE NOTES:

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