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    Ligation of TLR5 promotes myeloid cell infiltration and differentiation into mature osteoclasts in rheumatoid arthritis and experimental arthritis

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    Authors
    Kim, Seung-Jae
    Chen, Zhenlong
    Chamberlain, Nathan D.
    Essani, Abdul B.
    Volin, Michael V.
    Amin, M. Asif
    Volkov, Suncica
    Gravallese, Ellen M.
    Arami, Shiva
    Swedler, William
    Lane, Nancy E.
    Mehta, Anjali
    Sweiss, Nadera
    Shahrara, Shiva
    Show allShow less
    UMass Chan Affiliations
    Department of Medicine, Division of Rheumatology
    Document Type
    Journal Article
    Publication Date
    2014-10-15
    Keywords
    Animals
    Antibodies
    Arthritis, Experimental
    Arthritis, Rheumatoid
    Cell Differentiation
    Cell Movement
    Cells, Cultured
    Collagen
    Female
    Flagellin
    Humans
    Inflammation
    JNK Mitogen-Activated Protein Kinases
    Male
    Mice
    Mice, Inbred C57BL
    Mice, Inbred DBA
    Middle Aged
    Monocytes
    Myeloid Progenitor Cells
    NF-kappa B
    Osteoclasts
    Phosphatidylinositol 3-Kinases
    Phosphorylation
    Proto-Oncogene Proteins c-akt
    RANK Ligand
    Receptor Activator of Nuclear Factor-kappa B
    Synovial Fluid
    Toll-Like Receptor 5
    Tumor Necrosis Factor-alpha
    Cells
    Immunopathology
    Musculoskeletal Diseases
    Rheumatology
    Skin and Connective Tissue Diseases
    Show allShow less
    
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    Link to Full Text
    http://dx.doi.org/10.4049/jimmunol.1302998
    Abstract
    Our aim was to examine the impact of TLR5 ligation in rheumatoid arthritis (RA) and experimental arthritis pathology. Studies were conducted to investigate the role of TLR5 ligation on RA and mouse myeloid cell chemotaxis or osteoclast formation, and in addition, to uncover the significance of TNF-alpha function in TLR5-mediated pathogenesis. Next, the in vivo mechanism of action was determined in collagen-induced arthritis (CIA) and local joint TLR5 ligation models. Last, to evaluate the importance of TLR5 function in RA, we used anti-TLR5 Ab therapy in CIA mice. We show that TLR5 agonist, flagellin, can promote monocyte infiltration and osteoclast maturation directly through myeloid TLR5 ligation and indirectly via TNF-alpha production from RA and mouse cells. These two identified TLR5 functions are potentiated by TNF-alpha, because inhibition of both pathways can more strongly impair RA synovial fluid-driven monocyte migration and osteoclast differentiation compared with each factor alone. In preclinical studies, flagellin postonset treatment in CIA and local TLR5 ligation in vivo provoke homing and osteoclastic development of myeloid cells, which are associated with the TNF-alpha cascade. Conversely, CIA joint inflammation and bone erosion are alleviated when TLR5 function is blocked. We found that TLR5 and TNF-alpha pathways are interconnected, because TNF-alpha is produced by TLR5 ligation in RA myeloid cells, and anti-TNF-alpha therapy can markedly suppress TLR5 expression in RA monocytes. Our novel findings demonstrate that a direct and an indirect mechanism are involved in TLR5-driven RA inflammation and bone destruction.
    Source
    J Immunol. 2014 Oct 15;193(8):3902-13. doi: 10.4049/jimmunol.1302998. Epub 2014 Sep 8. Link to article on publisher's site
    DOI
    10.4049/jimmunol.1302998
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/48751
    PubMed ID
    25200955
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.4049/jimmunol.1302998
    Scopus Count
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