کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1929035 | 1050441 | 2012 | 6 صفحه PDF | دانلود رایگان |
TLR2 forms heterodimers with TLR1 and TLR6, and regulates host defense mechanisms against pathogens. We examined the role of TLR2 heterodimer signaling in osteoclast formation and inflammatory periodontitis. In co-cultures of mouse bone marrow cells and osteoblasts, a TLR2/6 ligand (diacylated lipopeptide designed from Gram-positive bacteria) markedly induced osteoclast formation. A TLR2/1 ligand (triacylated lipopeptide designed from Gram-negative bacteria) also induced osteoclast formation. The osteoclast formation induced by TLR2/6 and TLR2/1 ligands was completely suppressed by indomethacin. Osteoblasts expressed TLR1, 2, 4, and 6 mRNAs, and both TLR2/6 and TLR2/1 ligands induced the expression of COX-2, mPGES-1, and RANKL mRNA, as well as PGE production in osteoblasts. Both TLR2/6 and TLR2/1 ligands induced the resorption of mandibular alveolar bone in organ cultures, and elicited inflammatory periodontitis in vivo. Therefore, TLR2 heterodimer signaling may play a key role in PGE-mediated inflammatory bone loss in periodontal disease.
► We examine the role of TLR2 heterodimer signaling in bone metabolism.
► Both TLR2/6 ligand and TLR2/1 ligand markedly induce osteoclast formation in vitro.
► TLR2 heterodimer signaling induces the expression of COX-2 and mPGES-1 in osteoblasts.
► TLR2/6 and TLR2/1 ligands induce the resorption of mandibular alveolar bone in vitro.
► In mouse model, TLR2 heterodimer ligands elicit inflammatory periodontitis in vivo.
Journal: Biochemical and Biophysical Research Communications - Volume 428, Issue 1, 9 November 2012, Pages 110–115