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Article: Immunization enhances inflammation and tissue destruction in response to Porphyromonas gingivalis

TitleImmunization enhances inflammation and tissue destruction in response to Porphyromonas gingivalis
Authors
Issue Date2006
PublisherAmerican Society for Microbiology. The Journal's web site is located at http://iai.asm.org/
Citation
Infection And Immunity, 2006, v. 74 n. 4, p. 2286-2292 How to Cite?
AbstractIt is well established that host-bacterium interactions play a critical role in the initiation and progression of periodontal diseases. By the use of inhibitors, it has been shown that mediators associated with the innate immune response significantly contribute to the disease process. Less is known regarding the role of the acquired immune response. To investigate mechanisms by which the acquired immune response to Porphyromonas gingivalis could affect connective tissue, we used a well-documented calvarial model to study host-bacterium interactions. Injection of P. gingivalis stimulated gamma interferon, interleukin 6, macrophage inflammatory protein 2, and monocyte chemoattractant protein 1 expression as determined by real-time PCR. Prior immunization against P. gingivalis significantly enhanced the mRNA levels of these cytokines and chemokines. Similarly, immunization significantly increased and prolonged the formation of a polymorphonuclear leukocyte and mononuclear cell infiltrate (P < 0.05). In addition, the area of connective tissue destruction, osteoclastogenesis, bone loss, mRNA expression of proapoptotic genes, and degree of fibroblast apoptosis were increased in immunized mice (P < 0.05). These results indicate that activation of the acquired immunity by P. gingivalis increases the inflammatory and destructive responses which occur in part through up-regulating the innate immune response and enhancing osteoclastogenesis and fibroblast apoptosis. Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/154395
ISSN
2015 Impact Factor: 3.603
2015 SCImago Journal Rankings: 2.342
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeone, CWen_HK
dc.contributor.authorBokhadhoor, Hen_HK
dc.contributor.authorKuo, Den_HK
dc.contributor.authorDesta, Ten_HK
dc.contributor.authorYang, Jen_HK
dc.contributor.authorSiqueira, MFen_HK
dc.contributor.authorAmar, Sen_HK
dc.contributor.authorGraves, DTen_HK
dc.date.accessioned2012-08-08T08:25:05Z-
dc.date.available2012-08-08T08:25:05Z-
dc.date.issued2006en_HK
dc.identifier.citationInfection And Immunity, 2006, v. 74 n. 4, p. 2286-2292en_HK
dc.identifier.issn0019-9567en_HK
dc.identifier.urihttp://hdl.handle.net/10722/154395-
dc.description.abstractIt is well established that host-bacterium interactions play a critical role in the initiation and progression of periodontal diseases. By the use of inhibitors, it has been shown that mediators associated with the innate immune response significantly contribute to the disease process. Less is known regarding the role of the acquired immune response. To investigate mechanisms by which the acquired immune response to Porphyromonas gingivalis could affect connective tissue, we used a well-documented calvarial model to study host-bacterium interactions. Injection of P. gingivalis stimulated gamma interferon, interleukin 6, macrophage inflammatory protein 2, and monocyte chemoattractant protein 1 expression as determined by real-time PCR. Prior immunization against P. gingivalis significantly enhanced the mRNA levels of these cytokines and chemokines. Similarly, immunization significantly increased and prolonged the formation of a polymorphonuclear leukocyte and mononuclear cell infiltrate (P < 0.05). In addition, the area of connective tissue destruction, osteoclastogenesis, bone loss, mRNA expression of proapoptotic genes, and degree of fibroblast apoptosis were increased in immunized mice (P < 0.05). These results indicate that activation of the acquired immunity by P. gingivalis increases the inflammatory and destructive responses which occur in part through up-regulating the innate immune response and enhancing osteoclastogenesis and fibroblast apoptosis. Copyright © 2006, American Society for Microbiology. All Rights Reserved.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Microbiology. The Journal's web site is located at http://iai.asm.org/en_HK
dc.relation.ispartofInfection and Immunityen_HK
dc.subject.meshAdjuvants, Immunologic - Administration & Dosageen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBacterial Vaccines - Immunologyen_US
dc.subject.meshBacteroidaceae Infections - Immunology - Metabolism - Pathologyen_US
dc.subject.meshBone And Bones - Cytology - Metabolism - Pathologyen_US
dc.subject.meshChemokines - Biosynthesis - Geneticsen_US
dc.subject.meshCytokines - Biosynthesisen_US
dc.subject.meshImmunity, Activeen_US
dc.subject.meshInflammation - Immunology - Pathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshOsteoclasts - Metabolism - Pathologyen_US
dc.subject.meshPeriodontitis - Immunology - Metabolism - Pathologyen_US
dc.subject.meshPorphyromonas Gingivalis - Immunologyen_US
dc.titleImmunization enhances inflammation and tissue destruction in response to Porphyromonas gingivalisen_HK
dc.typeArticleen_HK
dc.identifier.emailKuo, D: davidkuo@hkucc.hku.hken_HK
dc.identifier.authorityKuo, D=rp00049en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1128/IAI.74.4.2286-2292.2006en_HK
dc.identifier.pmid16552059-
dc.identifier.scopuseid_2-s2.0-33645524540en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645524540&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume74en_HK
dc.identifier.issue4en_HK
dc.identifier.spage2286en_HK
dc.identifier.epage2292en_HK
dc.identifier.isiWOS:000236477000032-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLeone, CW=7101722164en_HK
dc.identifier.scopusauthoridBokhadhoor, H=12799341200en_HK
dc.identifier.scopusauthoridKuo, D=12800068200en_HK
dc.identifier.scopusauthoridDesta, T=6602863251en_HK
dc.identifier.scopusauthoridYang, J=36018056100en_HK
dc.identifier.scopusauthoridSiqueira, MF=12800330700en_HK
dc.identifier.scopusauthoridAmar, S=7005458479en_HK
dc.identifier.scopusauthoridGraves, DT=7201763199en_HK

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