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Periodontal therapy increases neutrophil extracellular trap degradation
In periodontitis, polymorphonuclear leucocytes (PMNs) are activated. They entrap and eliminate pathogens by releasing neutrophil extracellular traps (NETs). Abnormal NET degradation is part of a pro-inflammatory status, affecting co-morbidities such as cardiovascular disease. We aimed to investigate...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7903525/ https://www.ncbi.nlm.nih.gov/pubmed/31757174 http://dx.doi.org/10.1177/1753425919889392 |
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author | Moonen, Carolyn GJ Buurma, Kirsten GD Faruque, Mouri RJ Balta, Maria G Liefferink, Erol Bizzarro, Sergio Nicu, Elena A Loos, Bruno G |
author_facet | Moonen, Carolyn GJ Buurma, Kirsten GD Faruque, Mouri RJ Balta, Maria G Liefferink, Erol Bizzarro, Sergio Nicu, Elena A Loos, Bruno G |
author_sort | Moonen, Carolyn GJ |
collection | PubMed |
description | In periodontitis, polymorphonuclear leucocytes (PMNs) are activated. They entrap and eliminate pathogens by releasing neutrophil extracellular traps (NETs). Abnormal NET degradation is part of a pro-inflammatory status, affecting co-morbidities such as cardiovascular disease. We aimed to investigate the ex vivo NET degradation capacity of plasma from periodontitis patients compared to controls (part 1) and to quantify NET degradation before and after periodontal therapy (part 2). Fresh NETs were obtained by stimulating blood-derived PMNs with phorbol 12-myristate 13-acetate. Plasma samples from untreated periodontitis patients and controls were incubated for 3 h onto freshly generated NETs (part 1). Similarly, for part 2, NET degradation was studied for 91 patients before and 3, 6 and 12 mo after non-surgical periodontal therapy with and without adjunctive systemic antibiotics. Finally, NET degradation was fluorospectrometrically quantified. NET degradation levels did not differ between periodontitis patients and controls, irrespective of subject-related background characteristics. NET degradation significantly increased from 65.6 ± 1.7% before periodontal treatment to 75.7 ± 1.2% at 3 mo post periodontal therapy, and this improvement was maintained at 6 and 12 mo, irrespective of systemic usage of antibiotics. Improved NET degradation after periodontitis treatment is another systemic biomarker reflecting a decreased pro-inflammatory status, which also contributes to an improved cardiovascular condition. |
format | Online Article Text |
id | pubmed-7903525 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-79035252021-03-18 Periodontal therapy increases neutrophil extracellular trap degradation Moonen, Carolyn GJ Buurma, Kirsten GD Faruque, Mouri RJ Balta, Maria G Liefferink, Erol Bizzarro, Sergio Nicu, Elena A Loos, Bruno G Innate Immun Original Articles In periodontitis, polymorphonuclear leucocytes (PMNs) are activated. They entrap and eliminate pathogens by releasing neutrophil extracellular traps (NETs). Abnormal NET degradation is part of a pro-inflammatory status, affecting co-morbidities such as cardiovascular disease. We aimed to investigate the ex vivo NET degradation capacity of plasma from periodontitis patients compared to controls (part 1) and to quantify NET degradation before and after periodontal therapy (part 2). Fresh NETs were obtained by stimulating blood-derived PMNs with phorbol 12-myristate 13-acetate. Plasma samples from untreated periodontitis patients and controls were incubated for 3 h onto freshly generated NETs (part 1). Similarly, for part 2, NET degradation was studied for 91 patients before and 3, 6 and 12 mo after non-surgical periodontal therapy with and without adjunctive systemic antibiotics. Finally, NET degradation was fluorospectrometrically quantified. NET degradation levels did not differ between periodontitis patients and controls, irrespective of subject-related background characteristics. NET degradation significantly increased from 65.6 ± 1.7% before periodontal treatment to 75.7 ± 1.2% at 3 mo post periodontal therapy, and this improvement was maintained at 6 and 12 mo, irrespective of systemic usage of antibiotics. Improved NET degradation after periodontitis treatment is another systemic biomarker reflecting a decreased pro-inflammatory status, which also contributes to an improved cardiovascular condition. SAGE Publications 2019-11-22 2020-07 /pmc/articles/PMC7903525/ /pubmed/31757174 http://dx.doi.org/10.1177/1753425919889392 Text en © The Author(s) 2019 https://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Articles Moonen, Carolyn GJ Buurma, Kirsten GD Faruque, Mouri RJ Balta, Maria G Liefferink, Erol Bizzarro, Sergio Nicu, Elena A Loos, Bruno G Periodontal therapy increases neutrophil extracellular trap degradation |
title | Periodontal therapy increases neutrophil extracellular trap
degradation |
title_full | Periodontal therapy increases neutrophil extracellular trap
degradation |
title_fullStr | Periodontal therapy increases neutrophil extracellular trap
degradation |
title_full_unstemmed | Periodontal therapy increases neutrophil extracellular trap
degradation |
title_short | Periodontal therapy increases neutrophil extracellular trap
degradation |
title_sort | periodontal therapy increases neutrophil extracellular trap
degradation |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7903525/ https://www.ncbi.nlm.nih.gov/pubmed/31757174 http://dx.doi.org/10.1177/1753425919889392 |
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