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TLR5, a novel mediator of innate immunity-induced osteoclastogenesis and bone loss

Artikel i vetenskaplig tidskrift
Författare A. Kassem
Petra Henning
Bert Kindlund
Catharina Lindholm
Ulf H Lerner
Publicerad i Faseb Journal
Volym 29
Nummer/häfte 11
Sidor 4449-4460
ISSN 0892-6638
Publiceringsår 2015
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Centre for Bone and Arthritis Research
Sidor 4449-4460
Språk en
Länkar dx.doi.org/10.1096/fj.15-272559
Ämnesord inflammation, Toll-like receptors, osteoclasts, bone resorption, flagellin, toll-like-receptors, nf-kappa-b, rheumatoid-arthritis, signaling, pathways, in-vivo, resorption, cells, rankl, differentiation, lipopolysaccharide, Biochemistry & Molecular Biology, Life Sciences & Biomedicine - Other, Topics, Cell Biology
Ämneskategorier Immunologi inom det medicinska området, Endokrinologi

Sammanfattning

Accumulating evidence points to the importance of the innate immune system in inflammation-induced bone loss in infectious and autoimmune diseases. TLRs are well known for being activated by ligands expressed by bacteria, viruses, and fungi. Recent findings indicate that also endogenous ligands in inflammatory processes are important, one being a TLR5 agonist present in synovial fluid from patients with rheumatoid arthritis (RA). We found that activation of TLR5 by its specific ligand, flagellin, caused robust osteoclast formation and bone loss in cultured mouse neonatal parietal bones dependent on increased receptor activator of NF-kappa B ligand (RANKL): osteoprotegerin ratio, with half-maximal stimulation at 0.01 mu g/ml. Flagellin enhanced Rankl mRNA in isolated osteoblasts by a myeloid differentiation primary response gene 88 and NF-kappa B-dependent mechanism. Injection of flagellin locally over skull bones in 5-wk-oldmice resulted in increased mRNA expression of Rankl and osteoclastic genes, robust osteoclast formation, and bone loss. The effects in vitro and in vivo were absent in Tlr5(-/-) mice. These data show that TLR5 is a novel activator of RANKL and osteoclast formation and, therefore, a potential key factor in inflammation-induced bone erosions in diseases like RA, reactive arthritis, and periodontitis. TLR5 might be a promising novel treatment target for prevention of inflammatory bone loss.

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