Lack of chronic neuroinflammation in the absence of focal hemorrhage in a rat model of low-energy blast-induced TBI
| Autor: | Pierce Janssen, Miguel A. Gama Sosa, Fatemeh G. Haghighi, Georgina S. Perez Garcia, William G.M. Janssen, Danielle Vargas, Richard M. McCarron, Anna E. Tschiffely, Rita De Gasperi, Courtney Searcy, Stephen T. Ahlers, Heidi Sosa, Gregory A. Elder, Patrick R. Hof, Gissel M. Perez |
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| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
Male
Vascular Endothelial Growth Factor A 0301 basic medicine Pathology medicine.medical_specialty Traumatic brain injury medicine.medical_treatment Mice Transgenic tau Proteins Hippocampus Blast injury lcsh:RC346-429 Pathology and Forensic Medicine Lesion Mice 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine hemic and lymphatic diseases Brain Injuries Traumatic medicine Animals Chemokine CCL5 Macrophage inflammatory protein Blast wave Neuroinflammation lcsh:Neurology. Diseases of the nervous system Chemokine CCL3 Cerebral Cortex Microglia business.industry Research medicine.disease 3. Good health Mice Inbred C57BL Disease Models Animal 030104 developmental biology medicine.anatomical_structure Cytokine Mutation Cytokines Encephalitis Female Neurology (clinical) medicine.symptom business Intracranial Hemorrhages 030217 neurology & neurosurgery |
| Zdroj: | Acta Neuropathologica Communications, Vol 5, Iss 1, Pp 1-12 (2017) Acta Neuropathologica Communications |
| ISSN: | 2051-5960 |
| DOI: | 10.1186/s40478-017-0483-z |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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