Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury
Traumatic brain injury (TBI) is the principal cause of death and disability in children and young adults. Clinical and preclinical research efforts have been carried out to understand the acute, life-threatening pathophysiological events happening after TBI. In the past few years, however, it was re...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2019-11-01
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| Series: | Frontiers in Neuroscience |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fnins.2019.01178/full |
| _version_ | 1818361904300556288 |
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| author | Virginie Dinet Klaus G. Petry Jerome Badaut Jerome Badaut |
| author_facet | Virginie Dinet Klaus G. Petry Jerome Badaut Jerome Badaut |
| author_sort | Virginie Dinet |
| collection | DOAJ |
| description | Traumatic brain injury (TBI) is the principal cause of death and disability in children and young adults. Clinical and preclinical research efforts have been carried out to understand the acute, life-threatening pathophysiological events happening after TBI. In the past few years, however, it was recognized that TBI causes significant morbidity weeks, months, or years after the initial injury, thereby contributing substantially to the overall burden of TBI and the decrease of life expectancy in these patients. Long-lasting sequels of TBI include cognitive decline/dementia, sensory-motor dysfunction, and psychiatric disorders, and most important for patients is the need for socio-economic rehabilitation affecting their quality of life. Cerebrovascular alterations have been described during the first week after TBI for direct consequence development of neuroinflammatory process in relation to brain edema. Within the brain–immune interactions, the complement system, which is a family of blood and cell surface proteins, participates in the pathophysiology process. In fact, the complement system is part of the primary defense and clearance component of innate and adaptive immune response. In this review, the complement activation after TBI will be described in relation to the activation of the microglia and astrocytes as well as the blood–brain barrier dysfunction during the first week after the injury. Considering the neuroinflammatory activity as a causal element of neurological handicaps, some major parallel lines of complement activity in multiple sclerosis and Alzheimer pathologies with regard to cognitive impairment will be discussed for chronic TBI. A better understanding of the role of complement activation could facilitate the development of new therapeutic approaches for TBI. |
| first_indexed | 2024-12-13T21:24:06Z |
| format | Article |
| id | doaj.art-c48d0ab1ca8640b892e3c797227df3dd |
| institution | Directory Open Access Journal |
| issn | 1662-453X |
| language | English |
| last_indexed | 2024-12-13T21:24:06Z |
| publishDate | 2019-11-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neuroscience |
| spelling | doaj.art-c48d0ab1ca8640b892e3c797227df3dd2022-12-21T23:31:00ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2019-11-011310.3389/fnins.2019.01178487635Brain–Immune Interactions and Neuroinflammation After Traumatic Brain InjuryVirginie Dinet0Klaus G. Petry1Jerome Badaut2Jerome Badaut3INSERM U1029, Angiogenesis and Neuroinflammation Group, University of Bordeaux, Bordeaux, FranceINSERM U1029, Angiogenesis and Neuroinflammation Group, University of Bordeaux, Bordeaux, FranceCNRS UMR 5287, INCIA, Brain molecular Imaging Team, University of Bordeaux, Bordeaux, FranceDepartment of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA, United StatesTraumatic brain injury (TBI) is the principal cause of death and disability in children and young adults. Clinical and preclinical research efforts have been carried out to understand the acute, life-threatening pathophysiological events happening after TBI. In the past few years, however, it was recognized that TBI causes significant morbidity weeks, months, or years after the initial injury, thereby contributing substantially to the overall burden of TBI and the decrease of life expectancy in these patients. Long-lasting sequels of TBI include cognitive decline/dementia, sensory-motor dysfunction, and psychiatric disorders, and most important for patients is the need for socio-economic rehabilitation affecting their quality of life. Cerebrovascular alterations have been described during the first week after TBI for direct consequence development of neuroinflammatory process in relation to brain edema. Within the brain–immune interactions, the complement system, which is a family of blood and cell surface proteins, participates in the pathophysiology process. In fact, the complement system is part of the primary defense and clearance component of innate and adaptive immune response. In this review, the complement activation after TBI will be described in relation to the activation of the microglia and astrocytes as well as the blood–brain barrier dysfunction during the first week after the injury. Considering the neuroinflammatory activity as a causal element of neurological handicaps, some major parallel lines of complement activity in multiple sclerosis and Alzheimer pathologies with regard to cognitive impairment will be discussed for chronic TBI. A better understanding of the role of complement activation could facilitate the development of new therapeutic approaches for TBI.https://www.frontiersin.org/article/10.3389/fnins.2019.01178/fulltraumatic brain injuryneuroinflammationcomplementblood-brain barrierastrocyte |
| spellingShingle | Virginie Dinet Klaus G. Petry Jerome Badaut Jerome Badaut Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury Frontiers in Neuroscience traumatic brain injury neuroinflammation complement blood-brain barrier astrocyte |
| title | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
| title_full | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
| title_fullStr | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
| title_full_unstemmed | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
| title_short | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
| title_sort | brain immune interactions and neuroinflammation after traumatic brain injury |
| topic | traumatic brain injury neuroinflammation complement blood-brain barrier astrocyte |
| url | https://www.frontiersin.org/article/10.3389/fnins.2019.01178/full |
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