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*
Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Japan; and
Department of Periodontology, School of Dentistry, Aichi-Gakuin University, Chikusa-ku, Nagoya, Japan
Osteoclast differentiation factor (ODF), a recently
identified cytokine of the TNF family, is expressed as a
membrane-associated protein in osteoblasts and stromal cells. ODF
stimulates the differentiation of osteoclast precursors into
osteoclasts in the presence of M-CSF. Here we investigated the effects
of LPS on the gene expression of ODF in mouse osteoblasts and an
osteoblast cell line and found that LPS increased the ODF mRNA level. A
specific inhibitor of extracellular signal-regulated kinase or protein
kinase C inhibited this up-regulation, indicating that extracellular
signal-regulated kinase and protein kinase C activation was involved. A
protein synthesis inhibitor, cycloheximide, rather enhanced the
LPS-mediated increase of ODF mRNA, and both a neutralizing Ab of
TNF-
and a specific inhibitor of PGE synthesis failed to block the
ODF mRNA increase by native LPS. Thus, LPS directly induced ODF mRNA.
Mouse osteoblasts and an osteoblast cell line constitutively expressed
Toll-like receptor (TLR) 2 and 4, which are known as putative LPS
receptors. ODF mRNA increases in response to synthetic lipid A were
defective in primary osteoblasts from C3H/HeJ mice that contain a
nonfunctional mutation in the TLR4 gene, suggesting that
TLR4 plays an essential role in the process. Altogether, our results
indicate that ODF gene expression is directly increased in osteoblasts
by LPS treatment via TLR, and this pathway may play an important role
in the pathogenesis of LPS-mediated bone disorders, such as
periodontitis.
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