Mostra i principali dati dell'item
The Catabolic Role of Toll-Like Receptor 2 (TLR-2) Mediated by the NF-kappa B Pathway in Septic Arthritis
dc.creator | Papathanasiou, I. | en |
dc.creator | Malizos, K. N. | en |
dc.creator | Poultsides, L. | en |
dc.creator | Karachalios, T. | en |
dc.creator | Oikonomou, P. | en |
dc.creator | Tsezou, A. | en |
dc.date.accessioned | 2015-11-23T10:44:24Z | |
dc.date.available | 2015-11-23T10:44:24Z | |
dc.date.issued | 2011 | |
dc.identifier | 10.1002/jor.21239 | |
dc.identifier.issn | 0736-0266 | |
dc.identifier.uri | http://hdl.handle.net/11615/31939 | |
dc.description.abstract | Toll-like receptors (TLRs) are involved in mediating cell activation on stimulation with microbial components. Our objective was to investigate the role of 'PLR-2 mediated by the NF-kappa B pathway in septic arthritic chondrocytes. TLR-1, -2, and -6 mRNA expression levels were investigated in septic and normal chondrocytes using real-time reverse transcription-PCR. TLR-2 and MMP-13 mRNA and protein levels were measured using real-time PCR and Western blot analysis, respectively. Blocking TLR-2 mRNA expression was performed using small interfering-RNA (siRNA) against TLR-2 and subsequently MMP-3, MMP-13,1L-1 beta, and IL-6 mRNA levels, as well as p65 NF-kappa B, IkB alpha, and MMP-13 protein levels were evaluated using real-time PCR and Western blot analysis. IL-6 protein levels were measured using ELISA assay. We observed that TLR-1, -2, and -6 mRNA expression levels were significantly higher in septic compared to normal chondrocytes. MMP-13 mRNA and protein expressions were also significantly upregulated in septic arthritic cartilage. Blocking TLR-2 mRNA expression in septic chondrocytes resulted in significant increase of inactivated nonphosphorylatecl p65 NF-kappa B and IkB alpha protein levels and reduction in MMP-13, IL-1 beta, and IL-6 expression. Our findings suggest the pro-inflammatory and catabolic role of TLR-2 mediated by the NF-kappa B pathway in septic arthritis. Modulation of TLR-mediated signaling may be a potential therapeutic strategy for the prevention of postinfectious cartilage degradation in articular joints. (C) 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29: 247-251, 2011 | en |
dc.source | Journal of Orthopaedic Research | en |
dc.source.uri | <Go to ISI>://WOS:000286285900015 | |
dc.subject | septic arthritis | en |
dc.subject | chondrocytes | en |
dc.subject | TLR-2 | en |
dc.subject | MMP-13 | en |
dc.subject | IL-1 beta | en |
dc.subject | ARTICULAR CHONDROCYTES | en |
dc.subject | TRANSCRIPTION FACTORS | en |
dc.subject | RHEUMATOID-ARTHRITIS | en |
dc.subject | SYNOVIAL FIBROBLASTS | en |
dc.subject | SIGNALING PATHWAYS | en |
dc.subject | EXPRESSION | en |
dc.subject | CARTILAGE | en |
dc.subject | Orthopedics | en |
dc.title | The Catabolic Role of Toll-Like Receptor 2 (TLR-2) Mediated by the NF-kappa B Pathway in Septic Arthritis | en |
dc.type | journalArticle | en |
Files in questo item
Files | Dimensione | Formato | Mostra |
---|---|---|---|
Nessun files in questo item. |