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Infect. Immun., 09 1997, 3513-3519, Vol 65, No. 9
Y Miyata, H Takeda, S Kitano and S Hanazawa
In the present study, we examined mechanisms of Porphyromonas gingivalis
lipopolysaccharide (P-LPS)-stimulated bone resorption via CD14, one of the
lipopolysaccharide (LPS) receptors, and also assessed the inhibitory action
of several kinds of antibiotics on the LPS- induced stimulation. First, we
observed by using mouse embryonic calvarial cells that P-LPS stimulated
bone resorption through the action of endogenous interleukin-1beta
(IL-1beta) and interleukin-6 (IL- 6) via CD14 because (i) P-LPS-stimulated
expression of IL-1beta and IL- 6 genes in calvarial cells was inhibited by
an anti-mouse CD14 antibody, (ii) stimulated bone resorption was markedly
inhibited by both IL-1beta and IL-6 antibodies, and (iii) P-LPS-stimulated
bone resorption was clearly neutralized by an anti-mouse CD14 antibody.
Next, we examined the effects of several kinds of antibiotics on P-LPS-
stimulated bone resorption via CD14. Two of them, chloramphenicol and
erythromycin, inhibited P-LPS-stimulated bone resorption in a dose-
dependent manner. In an additional experiment, we observed that
chloramphenicol clearly inhibited P-LPS-stimulated expression of the CD14,
IL-1beta, and IL-6 genes in calvarial cells. These results suggest that
chloramphenicol might be a useful antibiotic as an anti- inflammatory agent
against P-LPS-stimulated periodontal destruction occurring via CD14 in
periodontal disease.
Copyright © 1997, American Society for Microbiology
Porphyromonas gingivalis lipopolysaccharide-stimulated bone resorption via CD14 is inhibited by broad-spectrum antibiotics
Department of Oral Microbiology, Meikai University School of Dentistry, Sakado City, Saitama, Japan.
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