Interleukin-1 and acute brain injury
Inflammation is the key host-defense response to infection and injury, yet also a major contributor to a diverse range of diseases, both peripheral and central in origin. Brain injury as a result of stroke or trauma is a leading cause of death and disability worldwide, yet there are no effective tre...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2015-02-01
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| Series: | Frontiers in Cellular Neuroscience |
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| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00018/full |
| _version_ | 1818339763183157248 |
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| author | Katie N Murray Adrian R Parry-Jones Stuart McRae Allan |
| author_facet | Katie N Murray Adrian R Parry-Jones Stuart McRae Allan |
| author_sort | Katie N Murray |
| collection | DOAJ |
| description | Inflammation is the key host-defense response to infection and injury, yet also a major contributor to a diverse range of diseases, both peripheral and central in origin. Brain injury as a result of stroke or trauma is a leading cause of death and disability worldwide, yet there are no effective treatments, resulting in enormous social and economic costs. Increasing evidence, both preclinical and clinical, highlights inflammation as an important factor in stroke, both in determining outcome and as a contributor to risk. A number of inflammatory mediators have been proposed as key targets for intervention to reduce the burden of stroke, several reaching clinical trial, but as yet yielding no success. Many factors could explain these failures, including the lack of robust preclinical evidence and poorly designed clinical trials, in addition to the complex nature of the clinical condition. Lack of consideration in preclinical studies of associated co-morbidities prevalent in the clinical stroke population is now seen as an important omission in previous work. These co-morbidities (atherosclerosis, hypertension, diabetes, infection) have a strong inflammatory component, supporting the need for greater understanding of how inflammation contributes to acute brain injury. Interleukin (IL)-1 is the prototypical pro-inflammatory cytokine, first identified many years ago as the endogenous pyrogen. Research over the last 20 years or so reveals that IL-1 is an important mediator of neuronal injury and blocking the actions of IL-1 is beneficial in a number of experimental models of brain damage. Mechanisms underlying the actions of IL-1 in brain injury remain unclear, though increasing evidence indicates the cerebrovasculature as a key target. Recent literature supporting this and other aspects of how IL-1 and systemic inflammation in general contribute to acute brain injury are discussed in this review. |
| first_indexed | 2024-12-13T15:32:10Z |
| format | Article |
| id | doaj.art-b37415d8b2104b7387773edc4d1ef23d |
| institution | Directory Open Access Journal |
| issn | 1662-5102 |
| language | English |
| last_indexed | 2024-12-13T15:32:10Z |
| publishDate | 2015-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cellular Neuroscience |
| spelling | doaj.art-b37415d8b2104b7387773edc4d1ef23d2022-12-21T23:40:08ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022015-02-01910.3389/fncel.2015.00018123775Interleukin-1 and acute brain injuryKatie N Murray0Adrian R Parry-Jones1Stuart McRae Allan2University of ManchesterSalford Royal NHS Foundation TrustUniversity of ManchesterInflammation is the key host-defense response to infection and injury, yet also a major contributor to a diverse range of diseases, both peripheral and central in origin. Brain injury as a result of stroke or trauma is a leading cause of death and disability worldwide, yet there are no effective treatments, resulting in enormous social and economic costs. Increasing evidence, both preclinical and clinical, highlights inflammation as an important factor in stroke, both in determining outcome and as a contributor to risk. A number of inflammatory mediators have been proposed as key targets for intervention to reduce the burden of stroke, several reaching clinical trial, but as yet yielding no success. Many factors could explain these failures, including the lack of robust preclinical evidence and poorly designed clinical trials, in addition to the complex nature of the clinical condition. Lack of consideration in preclinical studies of associated co-morbidities prevalent in the clinical stroke population is now seen as an important omission in previous work. These co-morbidities (atherosclerosis, hypertension, diabetes, infection) have a strong inflammatory component, supporting the need for greater understanding of how inflammation contributes to acute brain injury. Interleukin (IL)-1 is the prototypical pro-inflammatory cytokine, first identified many years ago as the endogenous pyrogen. Research over the last 20 years or so reveals that IL-1 is an important mediator of neuronal injury and blocking the actions of IL-1 is beneficial in a number of experimental models of brain damage. Mechanisms underlying the actions of IL-1 in brain injury remain unclear, though increasing evidence indicates the cerebrovasculature as a key target. Recent literature supporting this and other aspects of how IL-1 and systemic inflammation in general contribute to acute brain injury are discussed in this review.http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00018/fullInflammationInterleukin-1Neurogenesiscerebrovascular diseaseAcute brain injury |
| spellingShingle | Katie N Murray Adrian R Parry-Jones Stuart McRae Allan Interleukin-1 and acute brain injury Frontiers in Cellular Neuroscience Inflammation Interleukin-1 Neurogenesis cerebrovascular disease Acute brain injury |
| title | Interleukin-1 and acute brain injury |
| title_full | Interleukin-1 and acute brain injury |
| title_fullStr | Interleukin-1 and acute brain injury |
| title_full_unstemmed | Interleukin-1 and acute brain injury |
| title_short | Interleukin-1 and acute brain injury |
| title_sort | interleukin 1 and acute brain injury |
| topic | Inflammation Interleukin-1 Neurogenesis cerebrovascular disease Acute brain injury |
| url | http://journal.frontiersin.org/Journal/10.3389/fncel.2015.00018/full |
| work_keys_str_mv | AT katienmurray interleukin1andacutebraininjury AT adrianrparryjones interleukin1andacutebraininjury AT stuartmcraeallan interleukin1andacutebraininjury |