Editor: Artur Ulmer
Adiponectin inhibits osteoclast formation stimulated by lipopolysaccharide from Actinobacillus actinomycetemcomitans
Article first published online: 9 NOV 2006
FEMS Immunology & Medical Microbiology
Volume 49, Issue 1, pages 28–34, February 2007
How to Cite
Yamaguchi, N., Kukita, T., Li, Y.-J., Martinez Argueta, J. G., Saito, T., Hanazawa, S. and Yamashita, Y. (2007), Adiponectin inhibits osteoclast formation stimulated by lipopolysaccharide from Actinobacillus actinomycetemcomitans. FEMS Immunology & Medical Microbiology, 49: 28–34. doi: 10.1111/j.1574-695X.2006.00164.x
- Issue published online: 24 JAN 2007
- Article first published online: 9 NOV 2006
- Received 23 July 2006; revised 14 September 2006; accepted 15 September 2006.First published online 9 November 2006.
- periodontopathic bacteria;
- receptor activator of NF-κB ligand;
- nitric oxide
Previous epidemiologic studies have suggested that periodontal disease is closely related to obesity and glucose tolerance. As the level of adiponectin, an adipocyte-derived cytokine, in plasma had been reported to decrease in obese and type 2 diabetes patients, we explored the role of adiponectin in the etiology of periodontitis using the D clone of RAW264, a clone that exhibits highly efficient osteoclast formation, to determine whether adiponectin acts as a regulatory molecule in osteoclast formation stimulated by lipopolysaccharide of periodontopathic bacteria. We observed that adiponectin acted as a potent inhibitor of osteoclast formation stimulated by Toll-like receptor 4 (TLR4) ligand and receptor activator of NF-κB ligand (RANKL). Because NF-κB is an important transcription factor in osteoclast formation, we examined the effect of adiponectin on its transcriptional activity. A luciferase assay showed that adiponectin was able to inhibit the TLR4-mediated NF-κB activity in RAW264 cells. In addition, we observed that the cytokine was actually able to inhibit TLR4-mediated expression of the gene for inducible nitric oxide synthase and production of nitric oxide in the cells. These observations strongly suggest that adiponectin may function as a negative regulator of lipopolysaccharide/RANKL-mediated osteoclast formation in periodontal disease.