Abstract | OBJECTIVE: METHODS:
Interleukin-10 knockout (-/-) and wild-type mice were inoculated intraorally with P. gingivalis. Non-infected animals served as negative controls. Alveolar bone loss, gingival cytokine levels, and gingival gene expression were assessed using morphometric analysis, enzyme-linked immunosorbent assay (ELISA), and semiquantitative reverse transcription polymerase chain reaction (RT-PCR), respectively. RESULTS: CONCLUSION: The interleukin-10(-/-) mouse is highly susceptible to bone loss induced by the periodontal pathogen P. gingivalis, which is mediated via an interleukin-1-independent pathway.
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Authors | Hajime Sasaki, Yoshimasa Okamatsu, Toshihisa Kawai, Ralph Kent, Martin Taubman, Philip Stashenko |
Journal | Journal of periodontal research
(J Periodontal Res)
Vol. 39
Issue 6
Pg. 432-41
(Dec 2004)
ISSN: 0022-3484 [Print] United States |
PMID | 15491348
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Copyright | (c)Blackwell Munksgaard 2004 |
Chemical References |
- CD40 Antigens
- Carrier Proteins
- Interleukin-1
- Membrane Glycoproteins
- RANK Ligand
- Receptor Activator of Nuclear Factor-kappa B
- Tnfrsf11a protein, mouse
- Tnfsf11 protein, mouse
- Interleukin-10
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Topics |
- Alveolar Bone Loss
(microbiology)
- Analysis of Variance
- Animals
- Apoptosis
- CD40 Antigens
(biosynthesis)
- Carrier Proteins
(biosynthesis)
- Disease Models, Animal
- Gene Expression
- Genetic Predisposition to Disease
- Interleukin-1
(antagonists & inhibitors)
- Interleukin-10
(deficiency, genetics, physiology)
- Membrane Glycoproteins
(biosynthesis)
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Porphyromonas gingivalis
(pathogenicity)
- RANK Ligand
- Receptor Activator of Nuclear Factor-kappa B
- Specific Pathogen-Free Organisms
- Up-Regulation
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