Microenvironmental Variations After Blood-Brain Barrier Breakdown in Traumatic Brain Injury.

Yue Hu,Weiwei Tao

doi:10.3389/fnmol.2021.750810

Abstract

Traumatic brain injury (TBI) is linked to several pathologies. The blood-brain barrier (BBB) breakdown is considered to be one of the initial changes. Further, the microenvironmental alteration following TBI-induced BBB breakdown can be multi-scaled, constant, and dramatic. The microenvironmental variations after disruption of BBB includes several pathological changes, such as cerebral blood flow (CBF) alteration, brain edema, cerebral metabolism imbalances, and accumulation of inflammatory molecules. The modulation of the microenvironment presents attractive targets for TBI recovery, such as reducing toxic substances, inhibiting inflammation, and promoting neurogenesis. Herein, we briefly review the pathological alterations of the microenvironmental changes following BBB breakdown and outline potential interventions for TBI recovery based on microenvironmental modulation.

Highlights

Traumatic brain injury (TBI) is a critical public health problem in many areas worldwide, especially in the developed countries (Hydera et al, 2007; Corrigan et al, 2010; Roozenbeek et al, 2013)
The experiments in the TBI animal models have shown that the levels of IL-1β, IL-6, CXCL8, IL-10, and TNFα are chronically increased together with chronic microglial activation which link to neurodegeneration and dementia, suggesting that the inflammatory molecules accumulation in brain microenvironment following TBI may last for a long time
Understanding the underlying mechanisms of these variations after TBI are necessary in appropriate patient management (Lucke-Wold et al, 2015)

Summary

Introduction

Traumatic brain injury (TBI) is a critical public health problem in many areas worldwide, especially in the developed countries (Hydera et al, 2007; Corrigan et al, 2010; Roozenbeek et al, 2013). After traumatic brain injury (TBI), coverage rate of the pericytes dramatically decreased and diameter of capillary reduced, junction proteins were downregulated. Numerous findings from the animal TBI models have linked the endothelium cells to decreased CBF and poor outcome following brain injury.

Results

Conclusion