SAFETYLIT WEEKLY UPDATE

We compile citations and summaries of about 400 new articles every week.
Email Signup | RSS Feed

HELP: Tutorials | FAQ
CONTACT US: Contact info

Search Results

Journal Article

Citation

Gama Sosa MA, De Gasperi R, Perez Garcia GS, Sosa H, Searcy C, Vargas D, Janssen PL, Perez GM, Tschiffely AE, Janssen WG, McCarron RM, Hof PR, Haghighi FG, Ahlers ST, Elder GA. Acta Neuropathol. Commun. 2017; 5(1): e80.

Affiliation

Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Copyright

(Copyright © 2017, Holtzbrinck Springer Nature Publishing Group - BMC)

DOI

10.1186/s40478-017-0483-z

PMID

29126430

Abstract

Blast-related traumatic brain injury (TBI) has been a common cause of injury in the recent conflicts in Iraq and Afghanistan. Blast waves can damage blood vessels, neurons, and glial cells within the brain. Acutely, depending on the blast energy, blast wave duration, and number of exposures, blast waves disrupt the blood-brain barrier, triggering microglial activation and neuroinflammation. Recently, there has been much interest in the role that ongoing neuroinflammation may play in the chronic effects of TBI. Here, we investigated whether chronic neuroinflammation is present in a rat model of repetitive low-energy blast exposure. Six weeks after three 74.5-kPa blast exposures, and in the absence of hemorrhage, no significant alteration in the level of microglia activation was found. At 6 weeks after blast exposure, plasma levels of fractalkine, interleukin-1β, lipopolysaccharide-inducible CXC chemokine, macrophage inflammatory protein 1α, and vascular endothelial growth factor were decreased. However, no differences in cytokine levels were detected between blast-exposed and control rats at 40 weeks. In brain, isolated changes were seen in levels of selected cytokines at 6 weeks following blast exposure, but none of these changes was found in both hemispheres or at 40 weeks after blast exposure. Notably, one animal with a focal hemorrhagic tear showed chronic microglial activation around the lesion 16 weeks post-blast exposure. These findings suggest that focal hemorrhage can trigger chronic focal neuroinflammation following blast-induced TBI, but that in the absence of hemorrhage, chronic neuroinflammation is not a general feature of low-level blast injury.


Language: en

NEW SEARCH


All SafetyLit records are available for automatic download to Zotero & Mendeley
Print