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Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists
Periodontal ligament stem cells similarly to the mesenchymal stem cells of other tissues possess immunomodulatory properties, which are regulated by different cytokines, particularly by interferon-γ (IFN-γ). In contrast, less information is provided about the effect of toll-like receptors ligand on...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5634407/ https://www.ncbi.nlm.nih.gov/pubmed/28993635 http://dx.doi.org/10.1038/s41598-017-12480-7 |
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author | Andrukhov, Oleh Hong, Johanna Sang-A Andrukhova, Olena Blufstein, Alice Moritz, Andreas Rausch-Fan, Xiaohui |
author_facet | Andrukhov, Oleh Hong, Johanna Sang-A Andrukhova, Olena Blufstein, Alice Moritz, Andreas Rausch-Fan, Xiaohui |
author_sort | Andrukhov, Oleh |
collection | PubMed |
description | Periodontal ligament stem cells similarly to the mesenchymal stem cells of other tissues possess immunomodulatory properties, which are regulated by different cytokines, particularly by interferon-γ (IFN-γ). In contrast, less information is provided about the effect of toll-like receptors ligand on immunomodulatory properties of these cells. In the present study we investigated the response of human periodontal ligament stem cells (hPDLSCs) in response to simultaneous stimulation with IFN-γ and toll-like receptor (TLR) agonists. The resulting expression of indoleamine-2,3-dioxygenase-1 (IDO-1), interleukin (IL)-6, IL-8 and monocyte chemotactic protein 1 (MCP-1) was investigated. The expression of IDO-1 was upregulated by IFN-γ in both gene and protein levels. TLR2 agonists Pam3CSK4 induced gene expression of IDO-1, but had no effect on protein expression. IFN-γ induced IDO-1 protein expression was further enhanced by Pam3CSK4. TLR-4 agonist E. coli LPS has no significant effect on neither basal nor IFN-γ induced IDO-1 protein expression. The production of IL-6, IL-8, and MCP-1 was induced by TLR agonists. Neither basal nor TLR agonists induced production of these proteins was affected by IFN-γ. Our data shows potential interaction between IFN-γ and TLR2 responses in hPDLSCs, which might be involved in regulation of immune response in inflammatory diseases, and particularly periodontitis. |
format | Online Article Text |
id | pubmed-5634407 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-56344072017-10-18 Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists Andrukhov, Oleh Hong, Johanna Sang-A Andrukhova, Olena Blufstein, Alice Moritz, Andreas Rausch-Fan, Xiaohui Sci Rep Article Periodontal ligament stem cells similarly to the mesenchymal stem cells of other tissues possess immunomodulatory properties, which are regulated by different cytokines, particularly by interferon-γ (IFN-γ). In contrast, less information is provided about the effect of toll-like receptors ligand on immunomodulatory properties of these cells. In the present study we investigated the response of human periodontal ligament stem cells (hPDLSCs) in response to simultaneous stimulation with IFN-γ and toll-like receptor (TLR) agonists. The resulting expression of indoleamine-2,3-dioxygenase-1 (IDO-1), interleukin (IL)-6, IL-8 and monocyte chemotactic protein 1 (MCP-1) was investigated. The expression of IDO-1 was upregulated by IFN-γ in both gene and protein levels. TLR2 agonists Pam3CSK4 induced gene expression of IDO-1, but had no effect on protein expression. IFN-γ induced IDO-1 protein expression was further enhanced by Pam3CSK4. TLR-4 agonist E. coli LPS has no significant effect on neither basal nor IFN-γ induced IDO-1 protein expression. The production of IL-6, IL-8, and MCP-1 was induced by TLR agonists. Neither basal nor TLR agonists induced production of these proteins was affected by IFN-γ. Our data shows potential interaction between IFN-γ and TLR2 responses in hPDLSCs, which might be involved in regulation of immune response in inflammatory diseases, and particularly periodontitis. Nature Publishing Group UK 2017-10-09 /pmc/articles/PMC5634407/ /pubmed/28993635 http://dx.doi.org/10.1038/s41598-017-12480-7 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Andrukhov, Oleh Hong, Johanna Sang-A Andrukhova, Olena Blufstein, Alice Moritz, Andreas Rausch-Fan, Xiaohui Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists |
title | Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists |
title_full | Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists |
title_fullStr | Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists |
title_full_unstemmed | Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists |
title_short | Response of human periodontal ligament stem cells to IFN-γ and TLR-agonists |
title_sort | response of human periodontal ligament stem cells to ifn-γ and tlr-agonists |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5634407/ https://www.ncbi.nlm.nih.gov/pubmed/28993635 http://dx.doi.org/10.1038/s41598-017-12480-7 |
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