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Modulation of the Endocannabinoid System Following Central Nervous System Injury
Central nervous system (CNS) injury, such as stroke or trauma, is known to increase susceptibility to various infections that adversely affect patient outcomes (CNS injury-induced immunodepression—CIDS). The endocannabinoid system (ECS) has been shown to have immunoregulatory properties. Therefore,...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6359397/ https://www.ncbi.nlm.nih.gov/pubmed/30658442 http://dx.doi.org/10.3390/ijms20020388 |
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author | Zhou, Juan Noori, Haneen Burkovskiy, Ian Lafreniere, J. Daniel Kelly, Melanie E. M. Lehmann, Christian |
author_facet | Zhou, Juan Noori, Haneen Burkovskiy, Ian Lafreniere, J. Daniel Kelly, Melanie E. M. Lehmann, Christian |
author_sort | Zhou, Juan |
collection | PubMed |
description | Central nervous system (CNS) injury, such as stroke or trauma, is known to increase susceptibility to various infections that adversely affect patient outcomes (CNS injury-induced immunodepression—CIDS). The endocannabinoid system (ECS) has been shown to have immunoregulatory properties. Therefore, the ECS might represent a druggable target to overcome CIDS. Evidence suggests that cannabinoid type 2 receptor (CB(2)R) activation can be protective during the early pro-inflammatory phase after CNS injury, as it limits neuro-inflammation and, therefore, attenuates CIDS severity. In the later phase post CNS injury, CB(2)R inhibition is suggested as a promising pharmacologic strategy to restore immune function in order to prevent infection. |
format | Online Article Text |
id | pubmed-6359397 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-63593972019-02-06 Modulation of the Endocannabinoid System Following Central Nervous System Injury Zhou, Juan Noori, Haneen Burkovskiy, Ian Lafreniere, J. Daniel Kelly, Melanie E. M. Lehmann, Christian Int J Mol Sci Review Central nervous system (CNS) injury, such as stroke or trauma, is known to increase susceptibility to various infections that adversely affect patient outcomes (CNS injury-induced immunodepression—CIDS). The endocannabinoid system (ECS) has been shown to have immunoregulatory properties. Therefore, the ECS might represent a druggable target to overcome CIDS. Evidence suggests that cannabinoid type 2 receptor (CB(2)R) activation can be protective during the early pro-inflammatory phase after CNS injury, as it limits neuro-inflammation and, therefore, attenuates CIDS severity. In the later phase post CNS injury, CB(2)R inhibition is suggested as a promising pharmacologic strategy to restore immune function in order to prevent infection. MDPI 2019-01-17 /pmc/articles/PMC6359397/ /pubmed/30658442 http://dx.doi.org/10.3390/ijms20020388 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Zhou, Juan Noori, Haneen Burkovskiy, Ian Lafreniere, J. Daniel Kelly, Melanie E. M. Lehmann, Christian Modulation of the Endocannabinoid System Following Central Nervous System Injury |
title | Modulation of the Endocannabinoid System Following Central Nervous System Injury |
title_full | Modulation of the Endocannabinoid System Following Central Nervous System Injury |
title_fullStr | Modulation of the Endocannabinoid System Following Central Nervous System Injury |
title_full_unstemmed | Modulation of the Endocannabinoid System Following Central Nervous System Injury |
title_short | Modulation of the Endocannabinoid System Following Central Nervous System Injury |
title_sort | modulation of the endocannabinoid system following central nervous system injury |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6359397/ https://www.ncbi.nlm.nih.gov/pubmed/30658442 http://dx.doi.org/10.3390/ijms20020388 |
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