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Innate immune response to oral bacteria and the immune evasive characteristics of periodontal pathogens

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dc.contributor.authorJi, Suk-
dc.contributor.authorChoi, Youngnim-
dc.date.accessioned2021-09-06T04:45:04Z-
dc.date.available2021-09-06T04:45:04Z-
dc.date.created2021-06-14-
dc.date.issued2013-02-
dc.identifier.issn2093-2278-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/104071-
dc.description.abstractPeriodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherKOREAN ACAD PERIODONTOLOGY-
dc.subjectGINGIVAL EPITHELIAL-CELLS-
dc.subjectHUMAN POLYMORPHONUCLEAR LEUKOCYTES-
dc.subjectANTIMICROBIAL PEPTIDE EXPRESSION-
dc.subjectDENTICOLA SUPPRESSES EXPRESSION-
dc.subjectHUMAN BETA-DEFENSINS-
dc.subjectPORPHYROMONAS-GINGIVALIS-
dc.subjectTREPONEMA-DENTICOLA-
dc.subjectHUMAN BETA-DEFENSIN-2-
dc.subjectFUSOBACTERIUM-NUCLEATUM-
dc.subjectSIGNALING PATHWAYS-
dc.titleInnate immune response to oral bacteria and the immune evasive characteristics of periodontal pathogens-
dc.typeArticle-
dc.contributor.affiliatedAuthorJi, Suk-
dc.identifier.doi10.5051/jpis.2013.43.1.3-
dc.identifier.scopusid2-s2.0-84875910170-
dc.identifier.wosid000342342600002-
dc.identifier.bibliographicCitationJOURNAL OF PERIODONTAL AND IMPLANT SCIENCE, v.43, no.1, pp.3 - 11-
dc.relation.isPartOfJOURNAL OF PERIODONTAL AND IMPLANT SCIENCE-
dc.citation.titleJOURNAL OF PERIODONTAL AND IMPLANT SCIENCE-
dc.citation.volume43-
dc.citation.number1-
dc.citation.startPage3-
dc.citation.endPage11-
dc.type.rimsART-
dc.type.docTypeReview-
dc.identifier.kciidART001749177-
dc.description.journalClass1-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaDentistry, Oral Surgery & Medicine-
dc.relation.journalWebOfScienceCategoryDentistry, Oral Surgery & Medicine-
dc.subject.keywordPlusGINGIVAL EPITHELIAL-CELLS-
dc.subject.keywordPlusHUMAN POLYMORPHONUCLEAR LEUKOCYTES-
dc.subject.keywordPlusANTIMICROBIAL PEPTIDE EXPRESSION-
dc.subject.keywordPlusDENTICOLA SUPPRESSES EXPRESSION-
dc.subject.keywordPlusHUMAN BETA-DEFENSINS-
dc.subject.keywordPlusPORPHYROMONAS-GINGIVALIS-
dc.subject.keywordPlusTREPONEMA-DENTICOLA-
dc.subject.keywordPlusHUMAN BETA-DEFENSIN-2-
dc.subject.keywordPlusFUSOBACTERIUM-NUCLEATUM-
dc.subject.keywordPlusSIGNALING PATHWAYS-
dc.subject.keywordAuthorEpithelial cells-
dc.subject.keywordAuthorHost-pathogen interactions-
dc.subject.keywordAuthorImmune evasion-
dc.subject.keywordAuthorNeutrophils-
dc.subject.keywordAuthorPerodontitis-
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