Peripheral loss of EphA4 ameliorates TBI-induced neuroinflammation and tissue damage.

ABSTRACT:

Background

The continuum of pro- and anti-inflammatory response elicited by traumatic brain injury (TBI) is suggested to play a key role in the outcome of TBI; however, the underlying mechanisms remain ill -defined.

Methods

Here, we demonstrate that using bone marrow chimeric mice and systemic inhibition of EphA4 receptor shifts the pro-inflammatory milieu to pro-resolving following acute TBI.

Results

EphA4 expression is increased in the injured cortex as early as 2 h post-TBI and on CX3CR1^gfp-positive cells in the peri-lesion. Systemic inhibition or genetic deletion of EphA4 significantly reduced cortical lesion volume and shifted the inflammatory profile of peripheral-derived immune cells to pro-resolving in the damaged cortex. These findings were consist

SUBMITTER: Kowalski EA 

PROVIDER: S-EPMC6844068 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature