Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis.
Periodontitis is one of the most common infectious diseases in humans. It is characterized by a chronic inflammation of the tooth-supporting tissue that results in bone loss. However, the role and source of the pro-inflammatory cytokine interleukin-17 (IL-17) and of the cells producing it locally in...
| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2022-01-01
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| Series: | PLoS ONE |
| Online Access: | https://doi.org/10.1371/journal.pone.0265486 |
| _version_ | 1828824389363171328 |
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| author | Anneke Wilharm Christoph Binz Inga Sandrock Francesca Rampoldi Stefan Lienenklaus Eva Blank Andreas Winkel Abdi Demera Avi-Hai Hovav Meike Stiesch Immo Prinz |
| author_facet | Anneke Wilharm Christoph Binz Inga Sandrock Francesca Rampoldi Stefan Lienenklaus Eva Blank Andreas Winkel Abdi Demera Avi-Hai Hovav Meike Stiesch Immo Prinz |
| author_sort | Anneke Wilharm |
| collection | DOAJ |
| description | Periodontitis is one of the most common infectious diseases in humans. It is characterized by a chronic inflammation of the tooth-supporting tissue that results in bone loss. However, the role and source of the pro-inflammatory cytokine interleukin-17 (IL-17) and of the cells producing it locally in the gingiva is still controversial. Th17 αβ T cells, CD4+ exFoxP3+ αβ T cells, or IL-17-producing γδ T cells (γδ17 cells) seem to be decisive cellular players in periodontal inflammation. To address these issues in an experimental model for periodontitis, we employed genetic mouse models deficient for either γδ T cells or IL-17 cytokines and assessed the bone loss during experimental periodontal inflammation by stereomicroscopic, histological, and μCT-analysis. Furthermore, we performed flow-cytometric analyses and qPCR-analyses of the gingival tissue. We found no γδ T cell- or IL-17-dependent change in bone loss after four weeks of periodontitis. Apart from that, our data are complementary with earlier studies, which suggested IL-17-dependent aggravation of bone loss in early periodontitis, but a rather bone-protective role for IL-17 in late stages of experimental periodontitis with respect to the osteoclastogenicity defined by the RANKL/OPG ratio. |
| first_indexed | 2024-12-12T13:55:21Z |
| format | Article |
| id | doaj.art-64bbefb4b44b402c9ec7289cba7267ff |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-12T13:55:21Z |
| publishDate | 2022-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-64bbefb4b44b402c9ec7289cba7267ff2022-12-22T00:22:28ZengPublic Library of Science (PLoS)PLoS ONE1932-62032022-01-01173e026548610.1371/journal.pone.0265486Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis.Anneke WilharmChristoph BinzInga SandrockFrancesca RampoldiStefan LienenklausEva BlankAndreas WinkelAbdi DemeraAvi-Hai HovavMeike StieschImmo PrinzPeriodontitis is one of the most common infectious diseases in humans. It is characterized by a chronic inflammation of the tooth-supporting tissue that results in bone loss. However, the role and source of the pro-inflammatory cytokine interleukin-17 (IL-17) and of the cells producing it locally in the gingiva is still controversial. Th17 αβ T cells, CD4+ exFoxP3+ αβ T cells, or IL-17-producing γδ T cells (γδ17 cells) seem to be decisive cellular players in periodontal inflammation. To address these issues in an experimental model for periodontitis, we employed genetic mouse models deficient for either γδ T cells or IL-17 cytokines and assessed the bone loss during experimental periodontal inflammation by stereomicroscopic, histological, and μCT-analysis. Furthermore, we performed flow-cytometric analyses and qPCR-analyses of the gingival tissue. We found no γδ T cell- or IL-17-dependent change in bone loss after four weeks of periodontitis. Apart from that, our data are complementary with earlier studies, which suggested IL-17-dependent aggravation of bone loss in early periodontitis, but a rather bone-protective role for IL-17 in late stages of experimental periodontitis with respect to the osteoclastogenicity defined by the RANKL/OPG ratio.https://doi.org/10.1371/journal.pone.0265486 |
| spellingShingle | Anneke Wilharm Christoph Binz Inga Sandrock Francesca Rampoldi Stefan Lienenklaus Eva Blank Andreas Winkel Abdi Demera Avi-Hai Hovav Meike Stiesch Immo Prinz Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis. PLoS ONE |
| title | Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis. |
| title_full | Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis. |
| title_fullStr | Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis. |
| title_full_unstemmed | Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis. |
| title_short | Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis. |
| title_sort | interleukin 17 is disease promoting in early stages and protective in late stages of experimental periodontitis |
| url | https://doi.org/10.1371/journal.pone.0265486 |
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