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dc.contributor.authorZaric, Sen
dc.contributor.authorShelburne, Cen
dc.contributor.authorDarveau, Ren
dc.contributor.authorQuinn, DJen
dc.contributor.authorWeldon, Sen
dc.contributor.authorTaggart, CCen
dc.contributor.authorCoulter, WAen
dc.date.accessioned2016-05-12T13:07:02Z
dc.date.available2016-05-12T13:07:02Z
dc.date.issued2010-10en
dc.identifier.urihttp://hdl.handle.net/10026.1/4617
dc.description.abstract

Periodontitis, a chronic inflammatory disease of the tissues supporting the teeth, is characterized by an exaggerated host immune and inflammatory response to periopathogenic bacteria. Toll-like receptor activation, cytokine network induction, and accumulation of neutrophils at the site of inflammation are important in the host defense against infection. At the same time, induction of immune tolerance and the clearance of neutrophils from the site of infection are essential in the control of the immune response, resolution of inflammation, and prevention of tissue destruction. Using a human monocytic cell line, we demonstrate that Porphyromonas gingivalis lipopolysaccharide (LPS), which is a major etiological factor in periodontal disease, induces only partial immune tolerance, with continued high production of interleukin-8 (IL-8) but diminished secretion of tumor necrosis factor alpha (TNF-α) after repeated challenge. This cytokine response has functional consequences for other immune cells involved in the response to infection. Primary human neutrophils incubated with P. gingivalis LPS-treated naïve monocyte supernatant displayed a high migration index and increased apoptosis. In contrast, neutrophils treated with P. gingivalis LPS-tolerized monocyte supernatant showed a high migration index but significantly decreased apoptosis. Overall, these findings suggest that induction of an imbalanced immune tolerance in monocytes by P. gingivalis LPS, which favors continued secretion of IL-8 but decreased TNF-α production, may be associated with enhanced migration of neutrophils to the site of infection but also with decreased apoptosis and may play a role in the chronic inflammatory state seen in periodontal disease.

en
dc.format.extent4151 - 4156en
dc.languageengen
dc.language.isoengen
dc.subjectApoptosisen
dc.subjectCaspase 3en
dc.subjectCell Lineen
dc.subjectCell Movementen
dc.subjectGene Expression Regulationen
dc.subjectHumansen
dc.subjectImmune Toleranceen
dc.subjectInterleukin-8en
dc.subjectLipopolysaccharidesen
dc.subjectMembrane Potential, Mitochondrialen
dc.subjectNeutrophilsen
dc.subjectPorphyromonas gingivalisen
dc.subjectTumor Necrosis Factor-alphaen
dc.titleImpaired immune tolerance to Porphyromonas gingivalis lipopolysaccharide promotes neutrophil migration and decreased apoptosis.en
dc.typeJournal Article
plymouth.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/20679442en
plymouth.issue10en
plymouth.volume78en
plymouth.publication-statusPublisheden
plymouth.journalInfect Immunen
dc.identifier.doi10.1128/IAI.00600-10en
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/00 Groups by role
plymouth.organisational-group/Plymouth/00 Groups by role/Academics
plymouth.organisational-group/Plymouth/Faculty of Medicine and Dentistry
plymouth.organisational-group/Plymouth/Faculty of Medicine and Dentistry/Biomedical Research Group
plymouth.organisational-group/Plymouth/Faculty of Medicine and Dentistry/Biomedical Research Group/RC Reporting Group BRG
plymouth.organisational-group/Plymouth/Faculty of Medicine and Dentistry/Peninsula Dental School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Research Groups
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)
plymouth.organisational-group/Plymouth/Research Groups/Institute of Translational and Stratified Medicine (ITSMED)/CBR
dc.publisher.placeUnited Statesen
dc.identifier.eissn1098-5522en
dc.rights.embargoperiodNot knownen
rioxxterms.versionofrecord10.1128/IAI.00600-10en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.typeJournal Article/Reviewen


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