Inflammatory Regulation of CNS Barriers After Traumatic Brain Injury: A Tale Directed by Interleukin-1.

Autor:	Bodnar CN; Department of Neuroscience, University of Kentucky, Lexington, KY, United States.; Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY, United States., Watson JB; Department of Neuroscience, University of Kentucky, Lexington, KY, United States.; Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY, United States., Higgins EK; Department of Neuroscience, University of Kentucky, Lexington, KY, United States.; Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY, United States., Quan N; Department of Biomedical Science, Charles E. Schmidt College of Medicine and Brain Institute, Florida Atlantic University, Jupiter, FL, United States., Bachstetter AD; Department of Neuroscience, University of Kentucky, Lexington, KY, United States.; Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in immunology [Front Immunol] 2021 May 21; Vol. 12, pp. 688254. Date of Electronic Publication: 2021 May 21 (Print Publication: 2021).
DOI:	10.3389/fimmu.2021.688254
Abstrakt:	Several barriers separate the central nervous system (CNS) from the rest of the body. These barriers are essential for regulating the movement of fluid, ions, molecules, and immune cells into and out of the brain parenchyma. Each CNS barrier is unique and highly dynamic. Endothelial cells, epithelial cells, pericytes, astrocytes, and other cellular constituents each have intricate functions that are essential to sustain the brain's health. Along with damaging neurons, a traumatic brain injury (TBI) also directly insults the CNS barrier-forming cells. Disruption to the barriers first occurs by physical damage to the cells, called the primary injury. Subsequently, during the secondary injury cascade, a further array of molecular and biochemical changes occurs at the barriers. These changes are focused on rebuilding and remodeling, as well as movement of immune cells and waste into and out of the brain. Secondary injury cascades further damage the CNS barriers. Inflammation is central to healthy remodeling of CNS barriers. However, inflammation, as a secondary pathology, also plays a role in the chronic disruption of the barriers' functions after TBI. The goal of this paper is to review the different barriers of the brain, including (1) the blood-brain barrier, (2) the blood-cerebrospinal fluid barrier, (3) the meningeal barrier, (4) the blood-retina barrier, and (5) the brain-lesion border. We then detail the changes at these barriers due to both primary and secondary injury following TBI and indicate areas open for future research and discoveries. Finally, we describe the unique function of the pro-inflammatory cytokine interleukin-1 as a central actor in the inflammatory regulation of CNS barrier function and dysfunction after a TBI. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2021 Bodnar, Watson, Higgins, Quan and Bachstetter.)
Databáze:	MEDLINE
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