Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b
Background:Rosuvastatin exhibits anti-inflammatory effects and reduces periodontal diseases andatherosclerosis; however, its role in regulating periodontopathogen-induced endothelial proinflammatoryresponses remains unclear. The purpose of this study is to determine whether rosuvastatin can reduce t...
- Autores:
-
Gualtero, Diego Fernando
Viafara García, Sergio Marino
Morantes Medina, Sandra Johanna
Buitrago Ramírez, Diana Marcela
Gonzaléz, Octavio A.
Lafaurie, Gloria Ines
- Tipo de recurso:
- Article of journal
- Fecha de publicación:
- 2017
- Institución:
- Universidad El Bosque
- Repositorio:
- Repositorio U. El Bosque
- Idioma:
- eng
- OAI Identifier:
- oai:repositorio.unbosque.edu.co:20.500.12495/3390
- Acceso en línea:
- http://hdl.handle.net/20.500.12495/3390
https://doi.org/10.1902/jop.2016.160288
https://repositorio.unbosque.edu.co
- Palabra clave:
- Lipopolisacáridos
Periodontitis
Reacción en cadena de la polimerasa
Atherosclerosis
Immunity
Innate
- Rights
- openAccess
- License
- Acceso abierto
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oai:repositorio.unbosque.edu.co:20.500.12495/3390 |
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Repositorio U. El Bosque |
repository_id_str |
|
dc.title.spa.fl_str_mv |
Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b |
dc.title.translated.spa.fl_str_mv |
Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b |
title |
Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b |
spellingShingle |
Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b Lipopolisacáridos Periodontitis Reacción en cadena de la polimerasa Atherosclerosis Immunity Innate |
title_short |
Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b |
title_full |
Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b |
title_fullStr |
Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b |
title_full_unstemmed |
Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b |
title_sort |
Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype b |
dc.creator.fl_str_mv |
Gualtero, Diego Fernando Viafara García, Sergio Marino Morantes Medina, Sandra Johanna Buitrago Ramírez, Diana Marcela Gonzaléz, Octavio A. Lafaurie, Gloria Ines |
dc.contributor.author.none.fl_str_mv |
Gualtero, Diego Fernando Viafara García, Sergio Marino Morantes Medina, Sandra Johanna Buitrago Ramírez, Diana Marcela Gonzaléz, Octavio A. Lafaurie, Gloria Ines |
dc.contributor.orcid.none.fl_str_mv |
Lafaurie, Gloria Ines [0000-0003-3986-0625] Gualtero, Diego Fernando [0000-0002-6407-5605] Buitrago Ramírez, Diana Marcela [0000-0001-6283-7656] Viafara García, Sergio Marino [0000-0002-4208-1422] |
dc.subject.decs.spa.fl_str_mv |
Lipopolisacáridos Periodontitis Reacción en cadena de la polimerasa |
topic |
Lipopolisacáridos Periodontitis Reacción en cadena de la polimerasa Atherosclerosis Immunity Innate |
dc.subject.keywords.spa.fl_str_mv |
Atherosclerosis Immunity Innate |
description |
Background:Rosuvastatin exhibits anti-inflammatory effects and reduces periodontal diseases andatherosclerosis; however, its role in regulating periodontopathogen-induced endothelial proinflammatoryresponses remains unclear. The purpose of this study is to determine whether rosuvastatin can reduce theproinflammatory response induced byAggregatibacter actinomycetemcomitans(Aa) in human coronaryartery endothelial cells (HCAECs).Methods:HCAECs were stimulated with purifiedAaserotype b lipopolysaccharide (LPS) (Aa-LPS),heat-killed (HK) bacteria (Aa-HK), or live bacteria. Expression of Toll-like receptors and cellular adhesionmolecules were evaluated by fluorometric enzyme-linked immunosorbent assay. Endothelial cell activationwas evaluated by quantifying nuclear factor (NF)-kappa B-p65 and cytokine expression levels by quan-titative polymerase chain reaction and flow cytometry. Effect of rosuvastatin in expression of the athero-protective factor Kru ̈ppel-like factor 2 (KLF2) and cytokines were also studied using similar approaches.Results:HCAECs showed increased interleukin (IL)-6, IL-8, intercellular adhesion molecule 1, and plateletendothelial cell adhesion molecule 1 expression when stimulated withAa-LPS orAa-HK. NF-kB-p65 activa-tion was induced by all antigens.Aa-induced IL-6 and IL-8 production was inhibited by rosuvastatin, partic-ularly at higher doses. Interestingly, reduced IL-6 and IL-8 levels were observed in HCAECs stimulated withAain the presence of higher concentrations of rosuvastatin. This anti-inflammatory effect correlated witha significant increase of rosuvastatin-inducedKLF2.Conclusions:These results suggestAa-induced proinflammatory endothelial responses are regulatedby rosuvastatin in a mechanism that appears to involveKLF2activation. Use of rosuvastatin to preventcardiovascular disease may reduce risk of endothelial activation by bacterial antigens |
publishDate |
2017 |
dc.date.issued.none.fl_str_mv |
2017 |
dc.date.accessioned.none.fl_str_mv |
2020-07-09T19:42:21Z |
dc.date.available.none.fl_str_mv |
2020-07-09T19:42:21Z |
dc.type.coar.fl_str_mv |
http://purl.org/coar/resource_type/c_2df8fbb1 |
dc.type.coarversion.fl_str_mv |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
dc.type.local.none.fl_str_mv |
Artículo de revista |
dc.type.coar.none.fl_str_mv |
http://purl.org/coar/resource_type/c_6501 |
dc.type.driver.none.fl_str_mv |
info:eu-repo/semantics/article |
format |
http://purl.org/coar/resource_type/c_6501 |
dc.identifier.issn.none.fl_str_mv |
1943-3670 |
dc.identifier.uri.none.fl_str_mv |
http://hdl.handle.net/20.500.12495/3390 |
dc.identifier.doi.none.fl_str_mv |
https://doi.org/10.1902/jop.2016.160288 |
dc.identifier.instname.spa.fl_str_mv |
instname:Universidad El Bosque |
dc.identifier.reponame.spa.fl_str_mv |
reponame:Repositorio Institucional Universidad El Bosque |
dc.identifier.repourl.none.fl_str_mv |
https://repositorio.unbosque.edu.co |
identifier_str_mv |
1943-3670 instname:Universidad El Bosque reponame:Repositorio Institucional Universidad El Bosque |
url |
http://hdl.handle.net/20.500.12495/3390 https://doi.org/10.1902/jop.2016.160288 https://repositorio.unbosque.edu.co |
dc.language.iso.none.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartofseries.spa.fl_str_mv |
Journal of periodontology, 1943-3670, Vol. 88, Nro. 2, 2017, p. 225-235 |
dc.relation.uri.none.fl_str_mv |
https://aap.onlinelibrary.wiley.com/doi/abs/10.1902/jop.2016.160288 |
dc.rights.local.spa.fl_str_mv |
Acceso abierto |
dc.rights.accessrights.none.fl_str_mv |
http://purl.org/coar/access_right/c_abf2 info:eu-repo/semantics/openAccess Acceso abierto |
dc.rights.creativecommons.none.fl_str_mv |
2016-10-14 |
rights_invalid_str_mv |
Acceso abierto http://purl.org/coar/access_right/c_abf2 2016-10-14 |
eu_rights_str_mv |
openAccess |
dc.format.mimetype.none.fl_str_mv |
application/pdf |
dc.publisher.spa.fl_str_mv |
Wiley-Blackwell |
dc.publisher.journal.spa.fl_str_mv |
Journal of periodontology |
institution |
Universidad El Bosque |
bitstream.url.fl_str_mv |
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spelling |
Gualtero, Diego FernandoViafara García, Sergio MarinoMorantes Medina, Sandra JohannaBuitrago Ramírez, Diana MarcelaGonzaléz, Octavio A.Lafaurie, Gloria InesLafaurie, Gloria Ines [0000-0003-3986-0625]Gualtero, Diego Fernando [0000-0002-6407-5605]Buitrago Ramírez, Diana Marcela [0000-0001-6283-7656]Viafara García, Sergio Marino [0000-0002-4208-1422]2020-07-09T19:42:21Z2020-07-09T19:42:21Z20171943-3670http://hdl.handle.net/20.500.12495/3390https://doi.org/10.1902/jop.2016.160288instname:Universidad El Bosquereponame:Repositorio Institucional Universidad El Bosquehttps://repositorio.unbosque.edu.coapplication/pdfengWiley-BlackwellJournal of periodontologyJournal of periodontology, 1943-3670, Vol. 88, Nro. 2, 2017, p. 225-235https://aap.onlinelibrary.wiley.com/doi/abs/10.1902/jop.2016.160288Rosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype bRosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype bArtículo de revistahttp://purl.org/coar/resource_type/c_6501http://purl.org/coar/resource_type/c_2df8fbb1info:eu-repo/semantics/articlehttp://purl.org/coar/version/c_970fb48d4fbd8a85LipopolisacáridosPeriodontitisReacción en cadena de la polimerasaAtherosclerosisImmunityInnateBackground:Rosuvastatin exhibits anti-inflammatory effects and reduces periodontal diseases andatherosclerosis; however, its role in regulating periodontopathogen-induced endothelial proinflammatoryresponses remains unclear. The purpose of this study is to determine whether rosuvastatin can reduce theproinflammatory response induced byAggregatibacter actinomycetemcomitans(Aa) in human coronaryartery endothelial cells (HCAECs).Methods:HCAECs were stimulated with purifiedAaserotype b lipopolysaccharide (LPS) (Aa-LPS),heat-killed (HK) bacteria (Aa-HK), or live bacteria. Expression of Toll-like receptors and cellular adhesionmolecules were evaluated by fluorometric enzyme-linked immunosorbent assay. Endothelial cell activationwas evaluated by quantifying nuclear factor (NF)-kappa B-p65 and cytokine expression levels by quan-titative polymerase chain reaction and flow cytometry. Effect of rosuvastatin in expression of the athero-protective factor Kru ̈ppel-like factor 2 (KLF2) and cytokines were also studied using similar approaches.Results:HCAECs showed increased interleukin (IL)-6, IL-8, intercellular adhesion molecule 1, and plateletendothelial cell adhesion molecule 1 expression when stimulated withAa-LPS orAa-HK. NF-kB-p65 activa-tion was induced by all antigens.Aa-induced IL-6 and IL-8 production was inhibited by rosuvastatin, partic-ularly at higher doses. Interestingly, reduced IL-6 and IL-8 levels were observed in HCAECs stimulated withAain the presence of higher concentrations of rosuvastatin. This anti-inflammatory effect correlated witha significant increase of rosuvastatin-inducedKLF2.Conclusions:These results suggestAa-induced proinflammatory endothelial responses are regulatedby rosuvastatin in a mechanism that appears to involveKLF2activation. Use of rosuvastatin to preventcardiovascular disease may reduce risk of endothelial activation by bacterial antigensAcceso abiertohttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessAcceso abierto2016-10-14ORIGINALDiego F. Gualtero,Sergio M. Viafara-Garcia, Sandra J. Morantes_2017.pdfDiego F. Gualtero,Sergio M. Viafara-Garcia, Sandra J. Morantes_2017.pdfapplication/pdf1131421https://repositorio.unbosque.edu.co/bitstreams/7bb87cb8-fcc5-4c3d-83a5-5d136ed72c01/download4d21b2a88c6de50ac16428a5c2282ff4MD51LICENSElicense.txtlicense.txttext/plain; charset=utf-81748https://repositorio.unbosque.edu.co/bitstreams/5fe9c79c-c77f-46d7-a5d7-80c039e0d4d9/download8a4605be74aa9ea9d79846c1fba20a33MD52THUMBNAILDiego F. Gualtero,Sergio M. Viafara-Garcia, Sandra J. Morantes_2017.pdf.jpgDiego F. Gualtero,Sergio M. Viafara-Garcia, Sandra J. 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