TNF signaling is critical in mediating host response to infection caused by Porphyromonas gingivalis
Date
2001
DOI
Authors
Oskoui, Malekshah M.
Version
OA Version
Citation
Abstract
Lesions of endodontic origin are induced by pathogenic bacteria such as Porphyromonas gingivalis (P. gingivalis), which are recognized to stimulate an inflammatory response and lead to periapical bone destruction. P. gingivalis has been involved in the most common diseases of the oral cavity: periodontal disease, and lesions of endodontic origin. Both are considered to be initiated by bacteria that cause tissue damage, in part by activating the host response. Nonetheless, the mechanisms by which P. gingivalis causes tissue destruction have not been recognized.
To investigate one potential mechanism, we determined whether tumor necrosis factor (TNF) played a role in mediating soft and hard tissue damage caused by a mono-infection with P. gingivalis. TNF and IL-1, two potent pro-inflammatory cytokines, have been hypothesized to play a prominent role in this process. In our experiment, we tested the assumption that TNF and IL-1 activity is necessary for the recruitment of inflammatory cells such as PMNs and for the osteoclastogenesis that occurs after P. gingivalis infects mice. These experiments were performed in mice with targeted deletion of TNF receptors p55 and p75 or deletion of the IL-1 receptor type 1. Surprisingly, we found that the impact of each cytokine differed considerably. The results indicate that P. gingivalis induces each of the above mentioned events and that the extent of each is significantly reduced in TNF receptor -/- when compared to wild type mice. This is suggestive of up regulation of TNF by P. gingivalis infection, which contributes to both the dense connective tissue and bone destruction that occurs in periodontal and endodontic lesions.
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Thesis (MSD) --Boston University School of Dental Medicine, 2001 (Department of Endodontics).
Includes bibliographic references: leaves 52-63.
Thesis (MSD) --Boston University School of Dental Medicine, 2001 (Department of Endodontics).
Includes bibliographic references: leaves 52-63.
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This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.