CXCL5, CXCL8, and CXCL10 regulation by bacteria and mechanical forces in periodontium

Detalhes bibliográficos
Autor(a) principal: Rath-Deschner, Birgit
Data de Publicação: 2021
Outros Autores: 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.
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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spelling 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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