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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...

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Autores principales: Wilharm, Anneke, Binz, Christoph, Sandrock, Inga, Rampoldi, Francesca, Lienenklaus, Stefan, Blank, Eva, Winkel, Andreas, Demera, Abdi, Hovav, Avi-Hai, Stiesch, Meike, Prinz, Immo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8929577/
https://www.ncbi.nlm.nih.gov/pubmed/35298525
http://dx.doi.org/10.1371/journal.pone.0265486
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author Wilharm, Anneke
Binz, Christoph
Sandrock, Inga
Rampoldi, Francesca
Lienenklaus, Stefan
Blank, Eva
Winkel, Andreas
Demera, Abdi
Hovav, Avi-Hai
Stiesch, Meike
Prinz, Immo
author_facet Wilharm, Anneke
Binz, Christoph
Sandrock, Inga
Rampoldi, Francesca
Lienenklaus, Stefan
Blank, Eva
Winkel, Andreas
Demera, Abdi
Hovav, Avi-Hai
Stiesch, Meike
Prinz, Immo
author_sort Wilharm, Anneke
collection PubMed
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.
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spelling pubmed-89295772022-03-18 Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis Wilharm, Anneke Binz, Christoph Sandrock, Inga Rampoldi, Francesca Lienenklaus, Stefan Blank, Eva Winkel, Andreas Demera, Abdi Hovav, Avi-Hai Stiesch, Meike Prinz, Immo PLoS One Research Article 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. Public Library of Science 2022-03-17 /pmc/articles/PMC8929577/ /pubmed/35298525 http://dx.doi.org/10.1371/journal.pone.0265486 Text en © 2022 Wilharm et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Wilharm, Anneke
Binz, Christoph
Sandrock, Inga
Rampoldi, Francesca
Lienenklaus, Stefan
Blank, Eva
Winkel, Andreas
Demera, Abdi
Hovav, Avi-Hai
Stiesch, Meike
Prinz, Immo
Interleukin-17 is disease promoting in early stages and protective in late stages of experimental periodontitis
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
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8929577/
https://www.ncbi.nlm.nih.gov/pubmed/35298525
http://dx.doi.org/10.1371/journal.pone.0265486
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