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RESEARCH REPORT |
1 Department of Periodontology and
2 Department of Oral Biology, Faculty of Dental Medicine, Hadassah and Hebrew University Medical Centers, PO Box 12272, Jerusalem 91120, Israel;
*corresponding author, shapiral{at}cc.huji.ac.il
Infection with the periodontal pathogen Porphyromonas gingivalis causes a strong local inflammatory reaction. Using IFN
-deficient mice, we tested the hypothesis that the absence of IFN
would result in a reduction of the local pro-inflammatory response to P. gingivalis. Cytokine secretion by macrophages from IFN
-/- animals was significantly attenuated. Addition of IFN
restored cytokine secretion. In vivo injection of P. gingivalis into subcutaneous chambers increased the intra-chamber leukocyte counts and TNF
and IL-1ß levels. This increase was significantly lower in the IFN
-/- mice. Local reconstitution of IFN
-/- mice at the site of inflammation with the IFN
gene increased the levels of TNF
and decreased the IL-10 levels. Anti-P. gingivalis IgG1 levels, a marker of Th2 response, were higher in immunized IFN
-/- than in IFN
+/+ mice. The results suggest that lack of IFN
reduced the amplitude of the local pro-inflammatory response without decreasing the humoral protective response. The higher IgG1/IgG2a ratio observed supports the possibility of a Th2-dominant response in IFN
-deficient animals.
KEY WORDS: IFN
deficiency Porphyromonas gingivalis inflammation cytokines antibody
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