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Authordc.contributor.authorVicencio, Emiliano 
Authordc.contributor.authorCordero, Esteban M. 
Authordc.contributor.authorCortés, Bastián I. 
Authordc.contributor.authorPalominos, Sebastián 
Authordc.contributor.authorParra, Pedro 
Authordc.contributor.authorMella, Tania 
Authordc.contributor.authorHenrríquez, Constanza 
Authordc.contributor.authorSalazar, Nelda 
Authordc.contributor.authorMonasterio Ocares, Gustavo 
Authordc.contributor.authorCafferata, Emilio A. 
Authordc.contributor.authorMurgas, Paola 
Authordc.contributor.authorVernal Astudillo, Rolando 
Authordc.contributor.authorCortez, Cristian 
Admission datedc.date.accessioned2020-07-07T15:55:05Z
Available datedc.date.available2020-07-07T15:55:05Z
Publication datedc.date.issued2020
Cita de ítemdc.identifier.citationCells 2020, 9, 1221es_ES
Identifierdc.identifier.other10.3390/cells9051221
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/175829
Abstractdc.description.abstractThe adverse environmental conditions found in the periodontium during periodontitis pathogenesis stimulate local autophagy responses, mainly due to a continuous inflammatory response against the dysbiotic subgingival microbiome. The junctional epithelium represents the main site of the initial interaction between the host and the dysbiotic biofilm. Here, we investigated the role of autophagy in junctional epithelium keratinocytes (JEKs) in response to Aggregatibacter actinomycetemcomitans or its purified lipopolysaccharides (LPS). Immunofluorescence confocal analysis revealed an extensive nuclear translocation of transcription factor EB (TFEB) and consequently, an increase in autophagy markers and LC3-turnover assessed by immunoblotting and qRT-PCR. Correspondingly, challenged JEKs showed a punctuate cytosolic profile of LC3 protein contrasting with the diffuse distribution observed in untreated controls. Three-dimensional reconstructions of confocal images displayed a close association between intracellular bacteria and LC3-positive vesicles. Similarly, a close association between autophagic vesicles and the protein p62 was observed in challenged JEKs, indicating that p62 is the main adapter protein recruited during A. actinomycetemcomitans infection. Finally, the pharmacological inhibition of autophagy significantly increased the number of bacteria-infected cells as well as their death, similar to treatment with LPS. Our results indicate that A. actinomycetemcomitans infection induces autophagy in JEKs, and this homeostatic process has a cytoprotective effect on the host cells during the early stages of infection.es_ES
Patrocinadordc.description.sponsorshipChilean Governmental Agencia Nacional de Investigacion y Desarrollo (ANID) FONDECYT 11190073 FONDECYT 1181780 Universidad Mayores_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherMDPIes_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceCellses_ES
Keywordsdc.subjectJunctional epithelium keratinocyteses_ES
Keywordsdc.subjectA. actinomycetemcomitanses_ES
Keywordsdc.subjectLPSes_ES
Keywordsdc.subjectAutophagyes_ES
Keywordsdc.subjectLC3es_ES
Keywordsdc.subjectp62es_ES
Keywordsdc.subjectCell viabilityes_ES
Títulodc.titleAggregatibacter actinomycetemcomitans Induces Autophagy in Human Junctional Epithelium Keratinocyteses_ES
Document typedc.typeArtículo de revistaes_ES
dcterms.accessRightsdcterms.accessRightsAcceso Abierto
Catalogueruchile.catalogadorctces_ES
Indexationuchile.indexArtículo de publicación ISIes_ES


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile