Proton extrusion during oxidative burst in microglia exacerbates pathological acidosis following traumatic brain injury.

ABSTRACT: Acidosis is among the least studied secondary injury mechanisms associated with neurotrauma. Acute decreases in brain pH correlate with poor long-term outcome in patients with traumatic brain injury (TBI), however, the temporal dynamics and underlying mechanisms are unclear. As key drivers of neuroinflammation, we hypothesized that microglia directly regulate acidosis after TBI, and thereby, worsen neurological outcomes. Using a controlled cortical impact model in adult male mice we demonstrate that intracellular pH in microglia and extracellular pH surrounding the lesion site are significantly reduced for weeks after injury. Microglia proliferation and production of reactive oxygen species (ROS) were also increased during the first week, mirroring the increase in extracellular ROS levels

SUBMITTER: Ritzel RM 

PROVIDER: S-EPMC7819364 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature