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Injecting Immunosuppressive M2 Macrophages Alleviates the Symptoms of Periodontitis in Mice
Periodontitis is the second most common oral disease affecting tooth-supporting structures. The tissue damage is mainly initiated by the excessive secretion of proinflammatory cytokines by immune cells. Macrophages are a type of antigen-presenting cells that influence the adaptive immunity function....
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7645063/ https://www.ncbi.nlm.nih.gov/pubmed/33195441 http://dx.doi.org/10.3389/fmolb.2020.603817 |
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author | Miao, Yibin He, Liuting Qi, Xiaoyu Lin, Xiaoping |
author_facet | Miao, Yibin He, Liuting Qi, Xiaoyu Lin, Xiaoping |
author_sort | Miao, Yibin |
collection | PubMed |
description | Periodontitis is the second most common oral disease affecting tooth-supporting structures. The tissue damage is mainly initiated by the excessive secretion of proinflammatory cytokines by immune cells. Macrophages are a type of antigen-presenting cells that influence the adaptive immunity function. We used a unique set of cytokines, i.e., a combination of IL-4, IL-13, and IL-10, to stimulate macrophages into a subset of M2 polarization cells that express much higher levels of ARG-1, CD206, and PDL-2 genes. The cells’ anti-inflammatory potential was tested with mixed-lymphocyte reaction assay, which showed that this subset of macrophages could increase IL-2 secretion and suppress IL-17, IL-6, and TNF-α secretion by splenocytes. The gram-negative bacterial species Porphyromonas gingivalis was used to initiate an inflammatory process in murine periodontal tissues. In the meantime, cell injection therapy was used to dampen the excessive immune reaction and suppress osteoclast differentiation during periodontitis. Maxilla was collected and analyzed for osteoclast formation. The results indicated that mice in the cell injection group exhibited less osteoclast activity within the periodontal ligament region than in the periodontitis group. Moreover, the injection of M2 macrophages sustained the regulatory population ratio. Therefore, the M2 macrophages induced under the stimulation of IL-4, IL-13, and IL-10 combined had tremendous immune modulation ability. Injecting these cells into local periodontal tissue could effectively alleviate the symptom of periodontitis. |
format | Online Article Text |
id | pubmed-7645063 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-76450632020-11-13 Injecting Immunosuppressive M2 Macrophages Alleviates the Symptoms of Periodontitis in Mice Miao, Yibin He, Liuting Qi, Xiaoyu Lin, Xiaoping Front Mol Biosci Molecular Biosciences Periodontitis is the second most common oral disease affecting tooth-supporting structures. The tissue damage is mainly initiated by the excessive secretion of proinflammatory cytokines by immune cells. Macrophages are a type of antigen-presenting cells that influence the adaptive immunity function. We used a unique set of cytokines, i.e., a combination of IL-4, IL-13, and IL-10, to stimulate macrophages into a subset of M2 polarization cells that express much higher levels of ARG-1, CD206, and PDL-2 genes. The cells’ anti-inflammatory potential was tested with mixed-lymphocyte reaction assay, which showed that this subset of macrophages could increase IL-2 secretion and suppress IL-17, IL-6, and TNF-α secretion by splenocytes. The gram-negative bacterial species Porphyromonas gingivalis was used to initiate an inflammatory process in murine periodontal tissues. In the meantime, cell injection therapy was used to dampen the excessive immune reaction and suppress osteoclast differentiation during periodontitis. Maxilla was collected and analyzed for osteoclast formation. The results indicated that mice in the cell injection group exhibited less osteoclast activity within the periodontal ligament region than in the periodontitis group. Moreover, the injection of M2 macrophages sustained the regulatory population ratio. Therefore, the M2 macrophages induced under the stimulation of IL-4, IL-13, and IL-10 combined had tremendous immune modulation ability. Injecting these cells into local periodontal tissue could effectively alleviate the symptom of periodontitis. Frontiers Media S.A. 2020-10-23 /pmc/articles/PMC7645063/ /pubmed/33195441 http://dx.doi.org/10.3389/fmolb.2020.603817 Text en Copyright © 2020 Miao, He, Qi and Lin. https://creativecommons.org/licenses/by/4.0/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) and the copyright owner(s) 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 | Molecular Biosciences Miao, Yibin He, Liuting Qi, Xiaoyu Lin, Xiaoping Injecting Immunosuppressive M2 Macrophages Alleviates the Symptoms of Periodontitis in Mice |
title | Injecting Immunosuppressive M2 Macrophages Alleviates the Symptoms of Periodontitis in Mice |
title_full | Injecting Immunosuppressive M2 Macrophages Alleviates the Symptoms of Periodontitis in Mice |
title_fullStr | Injecting Immunosuppressive M2 Macrophages Alleviates the Symptoms of Periodontitis in Mice |
title_full_unstemmed | Injecting Immunosuppressive M2 Macrophages Alleviates the Symptoms of Periodontitis in Mice |
title_short | Injecting Immunosuppressive M2 Macrophages Alleviates the Symptoms of Periodontitis in Mice |
title_sort | injecting immunosuppressive m2 macrophages alleviates the symptoms of periodontitis in mice |
topic | Molecular Biosciences |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7645063/ https://www.ncbi.nlm.nih.gov/pubmed/33195441 http://dx.doi.org/10.3389/fmolb.2020.603817 |
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