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Mast Cell Deficiency Protects Mice from Surgery-Induced Neuroinflammation
Neuroinflammation plays a key role in the occurrence and development of neurodegenerative diseases. Microglia, the resident immune cells in the brain, have been recognized to contribute to neuroinflammation. Previous studies have shown that activated mast cells may be involved in surgery-induced neu...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7416247/ https://www.ncbi.nlm.nih.gov/pubmed/32801993 http://dx.doi.org/10.1155/2020/1921826 |
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author | Zhang, Xiang Dong, Hongquan Wang, Fei Zhang, Jun |
author_facet | Zhang, Xiang Dong, Hongquan Wang, Fei Zhang, Jun |
author_sort | Zhang, Xiang |
collection | PubMed |
description | Neuroinflammation plays a key role in the occurrence and development of neurodegenerative diseases. Microglia, the resident immune cells in the brain, have been recognized to contribute to neuroinflammation. Previous studies have shown that activated mast cells may be involved in surgery-induced neuroinflammation and neuronal apoptosis by using pharmacological methods. This study is aimed at ascertaining the exactly role of mast cells on neuroinflammation with the mast cell-deficient mice. Adult male C57BL6/J wild-type (WT) and mast cell-deficient (C57BL6/J KitWsh/Wsh (Wsh)) mice underwent tibial fracture surgery. Blood-brain barrier (BBB) breakdown, microglial activation, and neuroinflammatory levels were examined at 1 day after surgery. Surgery-induced BBB breakdown, microglial activation, and neuroinflammatory levels were significantly, pharmacologically reduced using a mast cell stabilizer, cromolyn sodium in WT mice (P < 0.05). These results were reproduced with mast cell deficiency. WT mice administered intraventricularly with cromolyn exhibited reduced BBB breakdown, microglial activation, and neuroinflammatory levels versus vehicle (P < 0.05). But there was no effect of cromolyn versus vehicle in Wsh mice, clarifying the specificity of cromolyn on brain mast cells. These findings demonstrated that activated mast cells promote surgery-induced BBB breakdown and neuroinflammation in mice, and open up a new therapeutic target for neuroinflammation-related diseases. |
format | Online Article Text |
id | pubmed-7416247 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-74162472020-08-14 Mast Cell Deficiency Protects Mice from Surgery-Induced Neuroinflammation Zhang, Xiang Dong, Hongquan Wang, Fei Zhang, Jun Mediators Inflamm Research Article Neuroinflammation plays a key role in the occurrence and development of neurodegenerative diseases. Microglia, the resident immune cells in the brain, have been recognized to contribute to neuroinflammation. Previous studies have shown that activated mast cells may be involved in surgery-induced neuroinflammation and neuronal apoptosis by using pharmacological methods. This study is aimed at ascertaining the exactly role of mast cells on neuroinflammation with the mast cell-deficient mice. Adult male C57BL6/J wild-type (WT) and mast cell-deficient (C57BL6/J KitWsh/Wsh (Wsh)) mice underwent tibial fracture surgery. Blood-brain barrier (BBB) breakdown, microglial activation, and neuroinflammatory levels were examined at 1 day after surgery. Surgery-induced BBB breakdown, microglial activation, and neuroinflammatory levels were significantly, pharmacologically reduced using a mast cell stabilizer, cromolyn sodium in WT mice (P < 0.05). These results were reproduced with mast cell deficiency. WT mice administered intraventricularly with cromolyn exhibited reduced BBB breakdown, microglial activation, and neuroinflammatory levels versus vehicle (P < 0.05). But there was no effect of cromolyn versus vehicle in Wsh mice, clarifying the specificity of cromolyn on brain mast cells. These findings demonstrated that activated mast cells promote surgery-induced BBB breakdown and neuroinflammation in mice, and open up a new therapeutic target for neuroinflammation-related diseases. Hindawi 2020-08-01 /pmc/articles/PMC7416247/ /pubmed/32801993 http://dx.doi.org/10.1155/2020/1921826 Text en Copyright © 2020 Xiang Zhang et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Zhang, Xiang Dong, Hongquan Wang, Fei Zhang, Jun Mast Cell Deficiency Protects Mice from Surgery-Induced Neuroinflammation |
title | Mast Cell Deficiency Protects Mice from Surgery-Induced Neuroinflammation |
title_full | Mast Cell Deficiency Protects Mice from Surgery-Induced Neuroinflammation |
title_fullStr | Mast Cell Deficiency Protects Mice from Surgery-Induced Neuroinflammation |
title_full_unstemmed | Mast Cell Deficiency Protects Mice from Surgery-Induced Neuroinflammation |
title_short | Mast Cell Deficiency Protects Mice from Surgery-Induced Neuroinflammation |
title_sort | mast cell deficiency protects mice from surgery-induced neuroinflammation |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7416247/ https://www.ncbi.nlm.nih.gov/pubmed/32801993 http://dx.doi.org/10.1155/2020/1921826 |
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