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...

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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
id UNBOSQUE2_4b7f97bf77b3b8009eab8c7d3b7e281e
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network_name_str 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
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dc.type.driver.none.fl_str_mv info:eu-repo/semantics/article
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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
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Acceso abierto
dc.rights.creativecommons.none.fl_str_mv 2016-10-14
rights_invalid_str_mv Acceso abierto
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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
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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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