CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium
Autor(a) principal: | |
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Data de Publicação: | 2021 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1016/j.aanat.2020.151648 http://hdl.handle.net/11449/206918 |
Resumo: | Objective: The aim of the present study was to evaluate the expressions of CXCL5, CXCL8, and CXCL10 in periodontal cells and tissues in response to microbial signals and/or biomechanical forces. Methods: Human gingival biopsies from inflamed and healthy sites were used to examine the chemokine expressions and protein levels by real-time PCR and immunohistochemistry. The chemokines were also investigated in gingival biopsies from rats submitted to experimental periodontitis and/or tooth movement. Furthermore, chemokine levels were determined in human periodontal fibroblasts stimulated by the periodontopathogen Fusobacterium nucleatum and/or constant tensile forces (CTS) by real-time PCR and ELISA. Additionally, gene expressions were evaluated in periodontal fibroblasts exposed to F. nucleatum and/or CTS in the presence and absence of a MAPK inhibitor by real-time PCR. Results: Increased CXCL5, CXCL8, and CXCL10 levels were observed in human and rat gingiva from sites of inflammation as compared with periodontal health. The rat experimental periodontitis caused a significant (p < 0.05) increase in alveolar bone resorption, which was further enhanced when combined with tooth movement. In vitro, F. nucleatum caused a significant upregulation of CXCL5, CXCL8, and CXCL10 at 1 day. Once the cells were exposed simultaneously to F. nucleatum and CTS, the chemokines regulation was significantly enhanced. The transcriptional findings were also observed at protein level. Pre-incubation with the MEK1/2 inhibitor significantly (p < 0.05) inhibited the stimulatory actions of F. nucleatum either alone or in combination with CTS on the expression levels of CXCL5, CXCL8, and CXCL10 at 1 d. Conclusions: Our data provide original evidence that biomechanical strain further increases the stimulatory actions of periodontal bacteria on the expressions of these chemokines. Therefore, biomechanical loading in combination with periodontal infection may lead to stronger recruitment of immunoinflammatory cells to the periodontium, which might result in an aggravation of periodontal inflammation and destruction. |
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CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontiumFusobacterium nucleatumGingivitisOrthodontic tooth movementPeriodontitisPeriodontiumObjective: The aim of the present study was to evaluate the expressions of CXCL5, CXCL8, and CXCL10 in periodontal cells and tissues in response to microbial signals and/or biomechanical forces. Methods: Human gingival biopsies from inflamed and healthy sites were used to examine the chemokine expressions and protein levels by real-time PCR and immunohistochemistry. The chemokines were also investigated in gingival biopsies from rats submitted to experimental periodontitis and/or tooth movement. Furthermore, chemokine levels were determined in human periodontal fibroblasts stimulated by the periodontopathogen Fusobacterium nucleatum and/or constant tensile forces (CTS) by real-time PCR and ELISA. Additionally, gene expressions were evaluated in periodontal fibroblasts exposed to F. nucleatum and/or CTS in the presence and absence of a MAPK inhibitor by real-time PCR. Results: Increased CXCL5, CXCL8, and CXCL10 levels were observed in human and rat gingiva from sites of inflammation as compared with periodontal health. The rat experimental periodontitis caused a significant (p < 0.05) increase in alveolar bone resorption, which was further enhanced when combined with tooth movement. In vitro, F. nucleatum caused a significant upregulation of CXCL5, CXCL8, and CXCL10 at 1 day. Once the cells were exposed simultaneously to F. nucleatum and CTS, the chemokines regulation was significantly enhanced. The transcriptional findings were also observed at protein level. Pre-incubation with the MEK1/2 inhibitor significantly (p < 0.05) inhibited the stimulatory actions of F. nucleatum either alone or in combination with CTS on the expression levels of CXCL5, CXCL8, and CXCL10 at 1 d. Conclusions: Our data provide original evidence that biomechanical strain further increases the stimulatory actions of periodontal bacteria on the expressions of these chemokines. Therefore, biomechanical loading in combination with periodontal infection may lead to stronger recruitment of immunoinflammatory cells to the periodontium, which might result in an aggravation of periodontal inflammation and destruction.Department of Orthodontics Center of Dento-Maxillo-Facial Medicine University of BonnSection of Experimental Dento-Maxillo-Facial Medicine Center of Dento-Maxillo-Facial Medicine University of BonnDepartment of Periodontology and Operative Dentistry University Medical Center of the Johannes Gutenberg UniversityDepartment of Diagnosis and Surgery School of Dentistry at Araraquara Sao Paulo State University UNESP AraraquaraDepartment of Periodontology Laboratory of Oral Microbiology University of BernDepartment of Orthodontics University Medical Centre of RegensburgDepartment of Diagnosis and Surgery School of Dentistry at Araraquara Sao Paulo State University UNESP AraraquaraUniversity of BonnUniversity Medical Center of the Johannes Gutenberg UniversityUniversidade Estadual Paulista (Unesp)University of BernUniversity Medical Centre of RegensburgRath-Deschner, BirgitMemmert, SvenjaDamanaki, Annade Molon, Rafael S. [UNESP]Nokhbehsaim, MarjanEick, SigrunKirschneck, ChristianCirelli, Joni A. [UNESP]Deschner, JamesJäger, AndreasNogueira, Andressa V.B.2021-06-25T10:46:01Z2021-06-25T10:46:01Z2021-03-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1016/j.aanat.2020.151648Annals of Anatomy, v. 234.1618-04020940-9602http://hdl.handle.net/11449/20691810.1016/j.aanat.2020.1516482-s2.0-85097107787Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengAnnals of Anatomyinfo:eu-repo/semantics/openAccess2021-10-23T15:41:29Zoai:repositorio.unesp.br:11449/206918Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T19:44:41.773777Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium |
title |
CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium |
spellingShingle |
CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium Rath-Deschner, Birgit Fusobacterium nucleatum Gingivitis Orthodontic tooth movement Periodontitis Periodontium |
title_short |
CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium |
title_full |
CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium |
title_fullStr |
CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium |
title_full_unstemmed |
CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium |
title_sort |
CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium |
author |
Rath-Deschner, Birgit |
author_facet |
Rath-Deschner, Birgit Memmert, Svenja Damanaki, Anna de Molon, Rafael S. [UNESP] Nokhbehsaim, Marjan Eick, Sigrun Kirschneck, Christian Cirelli, Joni A. [UNESP] Deschner, James Jäger, Andreas Nogueira, Andressa V.B. |
author_role |
author |
author2 |
Memmert, Svenja Damanaki, Anna de Molon, Rafael S. [UNESP] Nokhbehsaim, Marjan Eick, Sigrun Kirschneck, Christian Cirelli, Joni A. [UNESP] Deschner, James Jäger, Andreas Nogueira, Andressa V.B. |
author2_role |
author author author author author author author author author author |
dc.contributor.none.fl_str_mv |
University of Bonn University Medical Center of the Johannes Gutenberg University Universidade Estadual Paulista (Unesp) University of Bern University Medical Centre of Regensburg |
dc.contributor.author.fl_str_mv |
Rath-Deschner, Birgit Memmert, Svenja Damanaki, Anna de Molon, Rafael S. [UNESP] Nokhbehsaim, Marjan Eick, Sigrun Kirschneck, Christian Cirelli, Joni A. [UNESP] Deschner, James Jäger, Andreas Nogueira, Andressa V.B. |
dc.subject.por.fl_str_mv |
Fusobacterium nucleatum Gingivitis Orthodontic tooth movement Periodontitis Periodontium |
topic |
Fusobacterium nucleatum Gingivitis Orthodontic tooth movement Periodontitis Periodontium |
description |
Objective: The aim of the present study was to evaluate the expressions of CXCL5, CXCL8, and CXCL10 in periodontal cells and tissues in response to microbial signals and/or biomechanical forces. Methods: Human gingival biopsies from inflamed and healthy sites were used to examine the chemokine expressions and protein levels by real-time PCR and immunohistochemistry. The chemokines were also investigated in gingival biopsies from rats submitted to experimental periodontitis and/or tooth movement. Furthermore, chemokine levels were determined in human periodontal fibroblasts stimulated by the periodontopathogen Fusobacterium nucleatum and/or constant tensile forces (CTS) by real-time PCR and ELISA. Additionally, gene expressions were evaluated in periodontal fibroblasts exposed to F. nucleatum and/or CTS in the presence and absence of a MAPK inhibitor by real-time PCR. Results: Increased CXCL5, CXCL8, and CXCL10 levels were observed in human and rat gingiva from sites of inflammation as compared with periodontal health. The rat experimental periodontitis caused a significant (p < 0.05) increase in alveolar bone resorption, which was further enhanced when combined with tooth movement. In vitro, F. nucleatum caused a significant upregulation of CXCL5, CXCL8, and CXCL10 at 1 day. Once the cells were exposed simultaneously to F. nucleatum and CTS, the chemokines regulation was significantly enhanced. The transcriptional findings were also observed at protein level. Pre-incubation with the MEK1/2 inhibitor significantly (p < 0.05) inhibited the stimulatory actions of F. nucleatum either alone or in combination with CTS on the expression levels of CXCL5, CXCL8, and CXCL10 at 1 d. Conclusions: Our data provide original evidence that biomechanical strain further increases the stimulatory actions of periodontal bacteria on the expressions of these chemokines. Therefore, biomechanical loading in combination with periodontal infection may lead to stronger recruitment of immunoinflammatory cells to the periodontium, which might result in an aggravation of periodontal inflammation and destruction. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-06-25T10:46:01Z 2021-06-25T10:46:01Z 2021-03-01 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1016/j.aanat.2020.151648 Annals of Anatomy, v. 234. 1618-0402 0940-9602 http://hdl.handle.net/11449/206918 10.1016/j.aanat.2020.151648 2-s2.0-85097107787 |
url |
http://dx.doi.org/10.1016/j.aanat.2020.151648 http://hdl.handle.net/11449/206918 |
identifier_str_mv |
Annals of Anatomy, v. 234. 1618-0402 0940-9602 10.1016/j.aanat.2020.151648 2-s2.0-85097107787 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Annals of Anatomy |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
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1808129112611487744 |