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Periodontal Ligament Stem Cells Regulate Apoptosis of Neutrophils
Periodontal ligament stem cells (PDLSCs) are promising cell resource for the cell-based therapy for periodontitis and regeneration of bio-root. In this study, we investigated the effect of PDLSCs on neutrophil, a critical constituent of innate immunity, and the underlying mechanisms. The effect of P...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
De Gruyter Open
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5385971/ https://www.ncbi.nlm.nih.gov/pubmed/28401196 http://dx.doi.org/10.1515/med-2017-0004 |
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author | Wang, Qing Ding, Gang Xu, Xin |
author_facet | Wang, Qing Ding, Gang Xu, Xin |
author_sort | Wang, Qing |
collection | PubMed |
description | Periodontal ligament stem cells (PDLSCs) are promising cell resource for the cell-based therapy for periodontitis and regeneration of bio-root. In this study, we investigated the effect of PDLSCs on neutrophil, a critical constituent of innate immunity, and the underlying mechanisms. The effect of PDLSCs on the proliferation and apoptosis of resting neutrophils and IL-8 activated neutrophils was tested under cell-cell contact culture and Transwell culture, with or without anti-IL-6 neutralizing antibody. We found that PDLSCs could promote the proliferation and reduce the apoptosis of neutrophils whether under cell-cell contact or Transwell culture. Anti-IL-6 antibody reduced PDLSCs-mediated inhibition of neutrophil apoptosis. IL-6 at the concentration of 10ng/ml and 20ng/ml could inhibit neutrophil apoptosis statistically. Collectively, PDLSCs could reduce the apoptosis of neutrophils via IL-6. |
format | Online Article Text |
id | pubmed-5385971 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | De Gruyter Open |
record_format | MEDLINE/PubMed |
spelling | pubmed-53859712017-04-11 Periodontal Ligament Stem Cells Regulate Apoptosis of Neutrophils Wang, Qing Ding, Gang Xu, Xin Open Med (Wars) Regular Article Periodontal ligament stem cells (PDLSCs) are promising cell resource for the cell-based therapy for periodontitis and regeneration of bio-root. In this study, we investigated the effect of PDLSCs on neutrophil, a critical constituent of innate immunity, and the underlying mechanisms. The effect of PDLSCs on the proliferation and apoptosis of resting neutrophils and IL-8 activated neutrophils was tested under cell-cell contact culture and Transwell culture, with or without anti-IL-6 neutralizing antibody. We found that PDLSCs could promote the proliferation and reduce the apoptosis of neutrophils whether under cell-cell contact or Transwell culture. Anti-IL-6 antibody reduced PDLSCs-mediated inhibition of neutrophil apoptosis. IL-6 at the concentration of 10ng/ml and 20ng/ml could inhibit neutrophil apoptosis statistically. Collectively, PDLSCs could reduce the apoptosis of neutrophils via IL-6. De Gruyter Open 2017-03-06 /pmc/articles/PMC5385971/ /pubmed/28401196 http://dx.doi.org/10.1515/med-2017-0004 Text en © 2017 Qing Wang et al. http://creativecommons.org/licenses/by-nc-nd/3.0 This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License. |
spellingShingle | Regular Article Wang, Qing Ding, Gang Xu, Xin Periodontal Ligament Stem Cells Regulate Apoptosis of Neutrophils |
title | Periodontal Ligament Stem Cells Regulate Apoptosis of Neutrophils |
title_full | Periodontal Ligament Stem Cells Regulate Apoptosis of Neutrophils |
title_fullStr | Periodontal Ligament Stem Cells Regulate Apoptosis of Neutrophils |
title_full_unstemmed | Periodontal Ligament Stem Cells Regulate Apoptosis of Neutrophils |
title_short | Periodontal Ligament Stem Cells Regulate Apoptosis of Neutrophils |
title_sort | periodontal ligament stem cells regulate apoptosis of neutrophils |
topic | Regular Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5385971/ https://www.ncbi.nlm.nih.gov/pubmed/28401196 http://dx.doi.org/10.1515/med-2017-0004 |
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