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Strategies to increase the activity of microglia as efficient protectors of the brain against infections
In healthy individuals, infections of the central nervous system (CNS) are comparatively rare. Based on the ability of microglial cells to phagocytose and kill pathogens and on clinical findings in immunocompromised patients with CNS infections, we hypothesize that an intact microglial function is c...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033068/ https://www.ncbi.nlm.nih.gov/pubmed/24904283 http://dx.doi.org/10.3389/fncel.2014.00138 |
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author | Nau, Roland Ribes, Sandra Djukic, Marija Eiffert, Helmut |
author_facet | Nau, Roland Ribes, Sandra Djukic, Marija Eiffert, Helmut |
author_sort | Nau, Roland |
collection | PubMed |
description | In healthy individuals, infections of the central nervous system (CNS) are comparatively rare. Based on the ability of microglial cells to phagocytose and kill pathogens and on clinical findings in immunocompromised patients with CNS infections, we hypothesize that an intact microglial function is crucial to protect the brain from infections. Phagocytosis of pathogens by microglial cells can be stimulated by agonists of receptors of the innate immune system. Enhancing this pathway to increase the resistance of the brain to infections entails the risk of inducing collateral damage to the nervous tissue. The diversity of microglial cells opens avenue to selectively stimulate sub-populations responsible for the defence against pathogens without stimulating sub-populations which are responsible for collateral damage to the nervous tissue. Palmitoylethanolamide (PEA), an endogenous lipid, increased phagocytosis of bacteria by microglial cells in vitro without a measurable proinflammatory effect. It was tested clinically apparently without severe side effects. Glatiramer acetate increased phagocytosis of latex beads by microglia and monocytes, and dimethyl fumarate enhanced elimination of human immunodeficiency virus from infected macrophages without inducing a release of proinflammatory compounds. Therefore, the discovery of compounds which stimulate the elimination of pathogens without collateral damage of neuronal structures appears an achievable goal. PEA and, with limitations, glatiramer acetate and dimethyl fumarate appear promising candidates. |
format | Online Article Text |
id | pubmed-4033068 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-40330682014-06-05 Strategies to increase the activity of microglia as efficient protectors of the brain against infections Nau, Roland Ribes, Sandra Djukic, Marija Eiffert, Helmut Front Cell Neurosci Neuroscience In healthy individuals, infections of the central nervous system (CNS) are comparatively rare. Based on the ability of microglial cells to phagocytose and kill pathogens and on clinical findings in immunocompromised patients with CNS infections, we hypothesize that an intact microglial function is crucial to protect the brain from infections. Phagocytosis of pathogens by microglial cells can be stimulated by agonists of receptors of the innate immune system. Enhancing this pathway to increase the resistance of the brain to infections entails the risk of inducing collateral damage to the nervous tissue. The diversity of microglial cells opens avenue to selectively stimulate sub-populations responsible for the defence against pathogens without stimulating sub-populations which are responsible for collateral damage to the nervous tissue. Palmitoylethanolamide (PEA), an endogenous lipid, increased phagocytosis of bacteria by microglial cells in vitro without a measurable proinflammatory effect. It was tested clinically apparently without severe side effects. Glatiramer acetate increased phagocytosis of latex beads by microglia and monocytes, and dimethyl fumarate enhanced elimination of human immunodeficiency virus from infected macrophages without inducing a release of proinflammatory compounds. Therefore, the discovery of compounds which stimulate the elimination of pathogens without collateral damage of neuronal structures appears an achievable goal. PEA and, with limitations, glatiramer acetate and dimethyl fumarate appear promising candidates. Frontiers Media S.A. 2014-05-22 /pmc/articles/PMC4033068/ /pubmed/24904283 http://dx.doi.org/10.3389/fncel.2014.00138 Text en Copyright © 2014 Nau, Ribes, Djukic and Eiffert. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Nau, Roland Ribes, Sandra Djukic, Marija Eiffert, Helmut Strategies to increase the activity of microglia as efficient protectors of the brain against infections |
title | Strategies to increase the activity of microglia as efficient protectors of the brain against infections |
title_full | Strategies to increase the activity of microglia as efficient protectors of the brain against infections |
title_fullStr | Strategies to increase the activity of microglia as efficient protectors of the brain against infections |
title_full_unstemmed | Strategies to increase the activity of microglia as efficient protectors of the brain against infections |
title_short | Strategies to increase the activity of microglia as efficient protectors of the brain against infections |
title_sort | strategies to increase the activity of microglia as efficient protectors of the brain against infections |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033068/ https://www.ncbi.nlm.nih.gov/pubmed/24904283 http://dx.doi.org/10.3389/fncel.2014.00138 |
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