dc.creatorNavarrete, Mariely
dc.creatorGarcía, Jocelyn
dc.creatorDutzan, Nicolás
dc.creatorHenríquez, Leslie
dc.creatorPuente, Javier
dc.creatorCarvajal, Paola
dc.creatorHernandez, Marcela
dc.creatorGamonal Aravena, Jorge Antonio
dc.date.accessioned2018-12-20T15:24:46Z
dc.date.available2018-12-20T15:24:46Z
dc.date.created2018-12-20T15:24:46Z
dc.date.issued2014
dc.identifierJournal of Periodontology, Volumen 85, Issue 5, 2018, Pages 751-760
dc.identifier00223492
dc.identifier10.1902/jop.2013.130078
dc.identifierhttps://repositorio.uchile.cl/handle/2250/159097
dc.description.abstractMacrophages account for 5% to 30% of the inflammatory infiltrate in periodontitis and are activated by the classic and alternative pathways. These pathways are identified by indirect markers, among which interferon (IFN)-γ and interleukin-6 (IL)-6 of the classic pathway and IL-4 of the alternative pathway have been studied widely. Recently, factor XIII-A (FXIII-A) was reported to be a good marker of alternative pathway activation. The aim of this study is to determine the macrophage activation pathways involved in chronic periodontitis (CP) by the detection of the indirect markers IFN-γ, IL-6, FXIII-A, and IL-4. Methods: Biopsies were taken from patients with CP (n = 10) and healthy individuals (n = 10) for analysis of IFN-γ, IL-6, IL-4, and FXIII-A by Western blot (WB), immunohistochemistry (IHC), and enzyme-linked immunosorbent assay (ELISA). The same biopsies of healthy and diseased gingival tissue were used, and the expressions of these markers were compared between healthy individ
dc.languageen
dc.publisherAmerican Academy of Periodontology
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceJournal of Periodontology
dc.subjectCytokines
dc.subjectFactor XIII
dc.subjectImmunology
dc.subjectMacrophage activation
dc.subjectMacrophages
dc.subjectPeriodontal diseases
dc.titleInterferon-γ, interleukins-6 and -4, and factor XIII-A as indirect markers of the classical and alternative macrophage activation pathways in chronic periodontitis
dc.typeArtículo de revista


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