Dispensable role of myeloid differentiation primary response gene 88 (MyD88) and MyD88-dependent toll-like receptors (TLRs) in a murine model of osteoarthritis

Joint Bone Spine

Volumn 81, Issue 4, 2014, Pages 320-324

  Nasi, Sonia ^a   Ea, Hang Korng ^b,c   Chobaz, Véronique ^a   van Lent, Peter ^d   Lioté, Frédéric ^b,c   So, Alexander ^a   Busso, Nathalie ^a  

^a LAUSANNE UNIVERSITY HOSPITAL   (Switzerland)

^b HÔPITAL LARIBOISIÈRE   (France)

^c UNIVERSITÉ PARIS DESCARTES   (France)

^d RADBOUD UNIVERSITY NIJMEGEN   (Netherlands)

Author keywords

Cartilage degradation and metabolism; Chondrocytes apoptosis; Experimental osteoarthritis; MyD88; Synovial inflammation; TLRs

Indexed keywords

AGGRECAN; COLLAGEN TYPE 2; MATRIX METALLOPROTEINASE; MYELOID DIFFERENTIATION FACTOR 88; TOLL LIKE RECEPTOR 1; TOLL LIKE RECEPTOR 2; TOLL LIKE RECEPTOR 4; TOLL LIKE RECEPTOR 6; INTERLEUKIN 1 RECEPTOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; CARTILAGE; CARTILAGE CELL; CARTILAGE DEGENERATION; CELL MEMBRANE; CONTROLLED STUDY; DISEASE COURSE; FEMALE; HISTOPATHOLOGY; IMMUNOHISTOCHEMISTRY; INNATE IMMUNITY; JOINT INSTABILITY; KNEE MENISCUS; MENISCECTOMY; MOUSE; NONHUMAN; OARSI SCORING METHOD; OSTEOARTHRITIS; PATHOGENESIS; PROTEIN DEGRADATION; PROTEIN EXPRESSION; PROTEIN SYNTHESIS; SCORING SYSTEM; SHAM PROCEDURE; SYNOVITIS; SYNOVIUM; TISSUE METABOLISM; WILD TYPE; ANIMAL TISSUE; COLLAGEN SYNTHESIS; DISEASE SEVERITY; KNOCKOUT MOUSE; MURINE MODEL; MUSCULOSKELETAL DISEASE ASSESSMENT; OARSI SCORING; PROTEIN FUNCTION; SIGNAL TRANSDUCTION;

CARTILAGE DEGRADATION AND METABOLISM; CHONDROCYTES APOPTOSIS; EXPERIMENTAL OSTEOARTHRITIS; MYD88; SYNOVIAL INFLAMMATION; TLRS;

ANIMALS; CARTILAGE; DISEASE MODELS, ANIMAL; FEMALE; IMMUNITY, INNATE; INTERLEUKIN-1; JOINT INSTABILITY; MICE; MICE, KNOCKOUT; MYELOID DIFFERENTIATION FACTOR 88; OSTEOARTHRITIS, KNEE; SIGNAL TRANSDUCTION; TOLL-LIKE RECEPTORS;

EID: 84904099564     PISSN: 1297319X     EISSN: 17787254     Source Type: Journal    
DOI: 10.1016/j.jbspin.2014.01.018     Document Type: Article

References (32)

1. Goldring M.B. Update on the biology of the chondrocyte and new approaches to treating cartilage diseases. Best Pract Res Clin Rheumatol 2006, 20:1003-1025.
2. Loeser R.F., Goldring S.R., Scanzello C.R., et al. Osteoarthritis: a disease of the joint as an organ. Arthritis Rheum 2012, 64:1697-1707.
3. Abramson S.B., Attur M. Developments in the scientific understanding of osteoarthritis. Arthritis Res Ther 2009, 11:227.
4. McCarthy G.M., Cheung H.S. Point: hydroxyapatite crystal deposition is intimately involved in the pathogenesis and progression of human osteoarthritis. Curr Rheumatol Rep 2009, 11:141-147.
5. Goldring M.B., Goldring S.R. Osteoarthritis. J Cell Physiol 2007, 213:626-634.
6. Attur M., Belitskaya-Levy I., Oh C., et al. Increased interleukin-1beta gene expression in peripheral blood leukocytes is associated with increased pain and predicts risk for progression of symptomatic knee osteoarthritis. Arthritis Rheum 2011, 63:1908-1917.
7. Bondeson J., Blom A.B., Wainwright S., et al. The role of synovial macrophages and macrophage-produced mediators in driving inflammatory and destructive responses in osteoarthritis. Arthritis Rheum 2010, 62:647-657.
8. Daheshia M., Yao J.Q. The interleukin 1beta pathway in the pathogenesis of osteoarthritis. J Rheumatol 2008, 35:2306-2312.
9. Pujol J.P., Chadjichristos C., Legendre F., et al. Interleukin-1 and transforming growth factor-beta 1 as crucial factors in osteoarthritic cartilage metabolism. Connect Tissue Res 2008, 49:293-297.
10. McCormack W.J., Parker A.E., O'Neill L.A. Toll-like receptors and NOD-like receptors in rheumatic diseases. Arthritis Res Ther 2009, 11:243.
11. Piccinini A.M., Midwood K.S. DAMPening inflammation by modulating TLR signalling. Mediators Inflamm 2010, 2010:1-21.
12. Schroder K., Tschopp J. The inflammasomes. Cell 2010, 140:821-832.
13. Gross O., Thomas C.J., Guarda G., et al. The inflammasome: an integrated view. Immunol Rev 2011, 243:136-151.
14. Gross O., Yazdi A.S., Thomas C.J., et al. Inflammasome activators induce interleukin-1alpha secretion via distinct pathways with differential requirement for the protease function of caspase-1. Immunity 2012, 36:388-400.
15. Kamekura S., Hoshi K., Shimoaka T., et al. Osteoarthritis development in novel experimental mouse models induced by knee joint instability. Osteoarthritis Cartilage 2005, 13:632-641.
16. Pritzker K.P., Gay S., Jimenez S.A., et al. Osteoarthritis cartilage histopathology: grading and staging. Osteoarthritis Cartilage 2006, 14:13-29.
17. van Lent P.L., Blom A.B., Schelbergen R.F., et al. Active involvement of alarmins S100A8 and S100A9 in the regulation of synovial activation and joint destruction during mouse and human osteoarthritis. Arthritis Rheum 2012, 64:1466-1476.
18. Grimmer C., Balbus N., Lang U., et al. Regulation of type II collagen synthesis during osteoarthritis by prolyl-4-hydroxylases: possible influence of low oxygen levels. Am J Pathol 2006, 169:491-502.
19. Bobacz K., Sunk I.G., Hofstaetter J.G., et al. Toll-like receptors and chondrocytes: the lipopolysaccharide-induced decrease in cartilage matrix synthesis is dependent on the presence of toll-like receptor 4 and antagonized by bone morphogenetic protein 7. Arthritis Rheum 2007, 56:1880-1893.
20. Schelbergen R.F., Blom A.B., van den Bosch M.H., et al. Alarmins S100A8 and S100A9 elicit a catabolic effect in human osteoarthritic chondrocytes that is dependent on Toll-like receptor 4. Arthritis Rheum 2012, 64:1477-1487.
21. Kim H.A., Cho M.L., Choi H.Y., et al. The catabolic pathway mediated by Toll-like receptors in human osteoarthritic chondrocytes. Arthritis Rheum 2006, 54:2152-2163.
22. Sohn D.H., Sokolove J., Sharpe O., et al. Plasma proteins present in osteoarthritic synovial fluid can stimulate cytokine production via Toll-like receptor 4. Arthritis Res Ther 2012, 14:R7.
23. Blom A.B., van Lent P.L., Abdollahi-Roodsaz S., et al. Elusive role for Toll-like receptor 2 in joint pathology during experimental osteoarthritis. Osteoarthritis Cartilage 2011, 19:25. [Abstract].
24. Joosten L.A., Koenders M.I., Smeets R.L., et al. Toll-like receptor 2 pathway drives streptococcal cell wall-induced joint inflammation: critical role of myeloid differentiation factor 88. J Immunol 2003, 171:6145-6153.
25. Abdollahi-Roodsaz S., van de Loo F.A., Koenders M.I., et al. Destructive role of myeloid differentiation factor 88 and protective role of TRIF in interleukin-17-dependent arthritis in mice. Arthritis Rheum 2012, 64:1838-1847.
26. Liu-Bryan R., Scott P., Sydlaske A., et al. Innate immunity conferred by Toll-like receptors 2 and 4 and myeloid differentiation factor 88 expression is pivotal to monosodium urate monohydrate crystal-induced inflammation. Arthritis Rheum 2005, 52:2936-2946.
27. Pelletier J.P., Caron J.P., Evans C., et al. In vivo suppression of early experimental osteoarthritis by interleukin-1 receptor antagonist using gene therapy. Arthritis Rheum 1997, 40:1012-1019.
28. Iqbal I., Fleischmann R. Treatment of osteoarthritis with anakinra. Curr Rheumatol Rep 2007, 9:31-35.
29. Chevalier X., Conrozier T., Richette P. Desperately looking for the right target in osteoarthritis: the anti-IL-1 strategy. Arthritis Res Ther 2011, 13:124.
30. Jacques C., Gosset M., Berenbaum F., et al. The role of IL-1 and IL-1Ra in joint inflammation and cartilage degradation. Vitam Horm 2006, 74:371-403.
31. Clements K.M., Price J.S., Chambers M.G., et al. Gene deletion of either interleukin-1beta, interleukin-1beta-converting enzyme, inducible nitric oxide synthase, or stromelysin 1 accelerates the development of knee osteoarthritis in mice after surgical transection of the medial collateral ligament and partial medial meniscectomy. Arthritis Rheum 2003, 48:3452-3463.
32. Glasson S.S. In vivo osteoarthritis target validation utilizing genetically-modified mice. Curr Drug Targets 2007, 8:367-376.