Immunization Enhances Inflammation and Tissue Destruction in Response to Porphyromonas gingivalis
It 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...
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Published in | Infection and Immunity Vol. 74; no. 4; pp. 2286 - 2292 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Washington, DC
American Society for Microbiology
01.04.2006
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Subjects | |
Online Access | Get full text |
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Summary: | It 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this project. Editor: J. D. Clements Corresponding author. Mailing address: Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine, 700 Albany Street, W-201, Boston, MA 02118. Phone: (617) 638-4733. Fax: (617) 938-8837. E-mail: dgraves@bu.edu. |
ISSN: | 0019-9567 1098-5522 |
DOI: | 10.1128/iai.74.4.2286-2292.2006 |