title: Porphyromonas gingivalis lipopolysaccharide-stimulated bone resorption via CD14 is inhibited by broad-spectrum antibiotics.
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.
authors.affiliation: Department of Oral Microbiology, Meikai University School of Dentistry, Sakado City, Saitama, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Miyata
authors.forename: H
authors.initials: H
authors.lastname: Takeda
authors.forename: S
authors.initials: S
authors.lastname: Kitano
authors.forename: S
authors.initials: S
authors.lastname: Hanazawa
mesh_terms: D000667:Ampicillin / Q000494:pharmacology; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001862:Bone Resorption; D002701:Chloramphenicol / Q000494:pharmacology*; D004917:Erythromycin / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D007375:Interleukin-1 / Q000502:physiology; D015850:Interleukin-6 / Q000502:physiology; D018950:Lipopolysaccharide Receptors / Q000502:physiology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D051379:Mice; D010010:Osteoclasts / Q000378:metabolism; D016966:Porphyromonas gingivalis / Q000472:pathogenicity*; D012333:RNA, Messenger / Q000235:genetics; D012886:Skull; D013307:Streptomycin / Q000494:pharmacology; D013752:Tetracycline / Q000494:pharmacology
chemical_list: D000900:Anti-Bacterial Agents; D007375:Interleukin-1; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D004917:Erythromycin; D002701:Chloramphenicol; D000667:Ampicillin; D013752:Tetracycline; D013307:Streptomycin