Porphyromonas gingivalis lipopolysaccharide-stimulated bone resorption via CD14 is inhibited by broad-spectrum antibiotics

Infect Immun. 1997 Sep;65(9):3513-9. doi: 10.1128/iai.65.9.3513-3519.1997.

Abstract

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.

MeSH terms

  • Ampicillin / pharmacology
  • Animals
  • Anti-Bacterial Agents / pharmacology*
  • Bone Resorption*
  • Chloramphenicol / pharmacology*
  • Erythromycin / pharmacology*
  • Gene Expression / drug effects
  • Interleukin-1 / physiology
  • Interleukin-6 / physiology
  • Lipopolysaccharide Receptors / physiology*
  • Lipopolysaccharides / pharmacology*
  • Mice
  • Osteoclasts / metabolism
  • Porphyromonas gingivalis / pathogenicity*
  • RNA, Messenger / genetics
  • Skull
  • Streptomycin / pharmacology
  • Tetracycline / pharmacology

Substances

  • Anti-Bacterial Agents
  • Interleukin-1
  • Interleukin-6
  • Lipopolysaccharide Receptors
  • Lipopolysaccharides
  • RNA, Messenger
  • Erythromycin
  • Chloramphenicol
  • Ampicillin
  • Tetracycline
  • Streptomycin