Skip to main content Accessibility help
×
Hostname: page-component-77c89778f8-swr86 Total loading time: 0 Render date: 2024-07-17T00:18:01.976Z Has data issue: false hasContentIssue false

30 - Animal Models of Rheumatoid Arthritis

from PART VI - ANIMAL MODELS OF INFLAMMATION

Published online by Cambridge University Press:  05 April 2014

H.B. Patel
Affiliation:
Queen Mary College University of London
F. Humby
Affiliation:
Queen Mary College University of London
M. Blades
Affiliation:
University of London
C. Pitzalis
Affiliation:
Queen Mary College University of London
M. Seed
Affiliation:
University of London
Charles N. Serhan
Affiliation:
Harvard Medical School
Peter A. Ward
Affiliation:
University of Michigan, Ann Arbor
Derek W. Gilroy
Affiliation:
University College London
Get access

Summary

RHEUMATOID ARTHRITIS

Rheumatoid arthritis (RA) is an extremely painful, debilitating, and destructive inflammatory disease of diarthrodial joints. It affects between 0.5% and 1% of the world's population, with women having a threefold prevalence. Using traditional therapy, the majority will develop moderate disability at 2 years, with 40% being unable to work at 5 years. The disease has a high cost in pain, disability, and deformity. Morbidity is high, with a reduced lifespan. The advent of new treatment paradigms has meant that disability has been reduced, orthopedic surgeries have a much reduced rheumatoid joint replacement case-load, and whilst still severe, the aim of therapy is to preserve normal lifestyle and work patterns.

This is achieved by the use of low-dose methotrexate, leflunomide, or sulphasalazine, followed by biologic therapies, mainly anti-tumor necrosis factor (anti-TNF-α), anti-B cell (anti-CD20), recombinant human IL-1 receptor antagonist (rhIL-1ra), or anti-interleukin-6 (anti-IL-6). There remains a severe problem that despite these regimes a significant proportion (up to 40% for anti-TNF-α) do not respond. In addition, these treatments are expensive in their own right, and heavy on clinical resources for administration and monitoring. There is thus a continuing requirement for the development of improved therapeutics through drug discovery and further development of current therapeutics and their targets. A detailed understanding of the pathogenic mechanisms of RA are also required to fulfill these aims. Animal models of rheumatic disease continue to play a significant role in this process.

Type
Chapter
Information
Publisher: Cambridge University Press
Print publication year: 2010

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Cope, A.P. 2008. T cells in rheumatoid arthritis. Arthritis Res Ther 10(Suppl 1):S1.CrossRefGoogle ScholarPubMed
2. Silverman, G.J., and Boyle, D.L. 2008. Understanding the mechanistic basis in rheumatoid arthritis for clinical response to anti-CD20 therapy: the B-cell roadblock hypothesis. Immunol Rev 223:175–185.CrossRefGoogle ScholarPubMed
3. Moissec, P. 2008. Dynamic interactions between T cells and dendritic cells and their derived cytokines/chemokines in the rheumatoid synovium. Arthritis Res Ther 10(Suppl 1):S2.CrossRefGoogle Scholar
4. Brennan, F.M., and McInnes, I.B. 2008. Evidence that cytokines play a role in rheumatoid arthritis. J Clin Invest 118:3533–3546.CrossRefGoogle ScholarPubMed
5. Trentham, D.E., Townes, A.S., and Kang, A.H. 1977. Autoimmunity to type II collagen an experimental model of arthritis. J Exp Med 146(3):857–868.CrossRefGoogle ScholarPubMed
6. Luross, J.A., and Williams, N.A. 2001. The genetic and immunopathological processes underlying collagen-induced arthritis. Immunology 103(4):407–416.CrossRefGoogle ScholarPubMed
7. Holmdahl, R.H., Bockermann, R., Backlund, J., and Yamada, H. 2002. The molecular pathogenesis of collagen-induced arthritis in mice – a model for rheumatoid arthritis. Ageing Res Rev 1:135–147.CrossRefGoogle ScholarPubMed
8. Nandakumar, K.S., and Holmdahl, R. 2006. Antibody-induced arthritis: disease mechanisms and genes involved at the effector phase of arthritis. Arthritis Res Ther 8:223.CrossRefGoogle ScholarPubMed
9. Yanaba, K., Hamaguchi, Y., Venturi, G.M., Steeber, D.A., St. Clair, E.W., and Tedder, T.F. 2007. B cell depletion delays collagen-induced arthritis in mice: arthritis induction requires synergy between humoral and cell-mediated immunity. J Immunol. 179:1369–1380.CrossRefGoogle ScholarPubMed
10. Wooley, P.H. 2004. Immunotherapy in collagen-induced arthritis: past, present, and future. Am J Med Sci 327(4):217–226.CrossRefGoogle ScholarPubMed
11. Joosten, L.A., Helsen, M.M., Saxne, T., van De Loo, F.A., Heinegard, D., and van Den Berg, W.B. 1999. IL-1 alpha beta blockade prevents cartilage and bone destruction in murine type II collagen-induced arthritis, whereas TNF-alpha blockade only ameliorates joint inflammation. J Immunol 163(9):5049–5055.Google ScholarPubMed
12. Joosten, L.A., Helsen, M.M., van de Loo, F.A., and van den Berg, W.B. 2008. Anticytokine treatment of established type II collagen-induced arthritis in DBA/1 mice: a comparative study using anti-TNFalpha, anti-IL-1alpha/beta and IL-1Ra. Arthritis Rheum. 58(2 Suppl):S110–S122.Google ScholarPubMed
13. Kouskoff, V., Korganow, A.S., Duchatelle, V., Degott, C., Benoist, C., and Mathis, D. 1996. Organ-specific disease provoked by systemic autoimmunity. Cell 87(5):811–822.CrossRefGoogle ScholarPubMed
14. Kamradt, T., and Schubert, D. 2005. The role and clinical implications of G6PI in experimental models of rheumatoid arthritis. Arthritis Res Ther 7(1):20–28.CrossRefGoogle ScholarPubMed
15. Griffiths, R.J. 1992. Characterisation and pharmacological sensitivity of antigen arthritis induced by methylated bovine serum albumin in the rat. Inflamm Res 35(1–2):88–95.Google ScholarPubMed
16. Staite, N.D., Cutshaw, L.G., Dunn, C.J. 1989. The effects of different sensitisation protocols on arthritic responses in antigen-induced arthritis. Inflamm Res 27:338–340.Google Scholar
17. Van Den Berg., W., Van Beusekom., H.J., Van De Putte., L.B.A., Zwarts, W.A., and Van Der Sluis, M. 1982. Antigen handling in antigen-induced arthritis in mice an autoradiographic and immunofluorescence study using whole joint sections. Am J Pathol 108:9–16.Google ScholarPubMed
18. Crossley, M.J., Spowage, M., and Hunneyball, I.M. 1987. Studies on the effects of pharmacological agents on antigen-induced arthritis in BALB/c mice. Drugs Exp Clin Res 13(5):273–277.Google ScholarPubMed
19. Seed, M.P. 2003. The assessment of inflammation, cartilage matrix and bone loss in experimental mono-articular arthritis in the rat. Methods Mol Biol 225:161–174.Google Scholar
20. Woodruff, T.M., Strachan, A.J., Dryburgh, N., et al. 2002. Antiarthritic activity of an orally active c5a receptor antagonist against antigen-induced monarticular arthritis in the rat. Arthritis Rheum 46:2476–2485.CrossRefGoogle ScholarPubMed
21. Pohlers, D., Siegling, A., Buchner, E., et al. 2005. Expression of cytokine mRNA and protein in joints and lymphoid organs during the course of rat antigen-induced arthritis. Arthritis Res Ther 7:R445–R457.CrossRefGoogle ScholarPubMed
22. Seed, M.P., and Gardner, C.R. 2005. The modulation of intra-articular inflammation, cartilage matrix and bone loss in mono-articular arthritis induced by heat-killed Myobacterium tuberculosis. Inflammopharmacology 12(5–6):551–567.CrossRefGoogle Scholar
23. Davis, L.S., Sackler, M., Brezinschek, R.I., et al. 2002. Inflammation, immune reactivity, and angiogenesis in a severe combined immunodeficiency model of rheumatoid arthritis. Am J Pathol 160:357–367.CrossRefGoogle Scholar
24. Wahid, S., Blades, M.C., De Lord, D., et al. 2000. Tumour necrosis factor-alpha (TNF-a) enhances lymphocyte migration into rheumatoid synovial tissue transplanted into severe combined immunodeficient (SCID) mice. Clin Exp Immunol 122:133–142.CrossRefGoogle Scholar
25. Humby, F., Bombardieri, M., Manzo, A., et al. 2009. Ectopic lymphoid structures support ongoing production of class switched autoantibodies in rheumatoid syn-ovium. PLoS Med 6(1):e1.CrossRefGoogle Scholar
26. Schopf, L., Anderson, K., and Jaffe, B.D. 2006. Rat models of arthritis: similarities, differences, advantages and disadvantages in the identification of novel therapeutics. In: In vivo Models of Inflammation. Progress in Inflammation Research. Parnham, M.J. (ed.), 2nd Ed., Vol 1., pp. 1–34. Basel: Birkhauser.Google Scholar
27. Koenders, M.I., Kolls, J.K., Oppers-Walgreen, B., et al. 2005. Interleukin-17 receptor deficiency results in impaired synovial expression of interleukin-1 and matrix metalloproteinases 3, 9, and 13 and prevents cartilage destruction during chronic reactivated strep-tococcal cell wall-induced arthritis. Arthritis Rheum 52:3239–3247.CrossRefGoogle ScholarPubMed
28. van den Broek, M.F. 1989. Streptococcal cell wall-induced polyarthritis in the rat. Mechanisms for chronicity and regulation of susceptibility. APMIS 97:861–878.Google Scholar
29. van Bruggen, M.C., van den Broek, M.F., and van den Berg, W.B. 1991. Streptococcal cell wall-induced arthritis and adjuvant arthritis in F344 – Lewis and in Lewis – F344 bone marrow chimeras. Cell Immunol 136(2):278–290.CrossRefGoogle ScholarPubMed
30. Holmdahl, R., Lorentzen, J.C., Lu, S., et al. 2001. Arthritis induced in rats with non-immunogenic adjuvants as models for rheumatoid arthritis. Immunol Rev 184:184–202.CrossRefGoogle Scholar
31. Hoffmann, M.H., Tuncel, J., Skriner, K., et al. 2007. The rheumatoid arthritis-associated autoantigen hnRNP-A2 (RA33) is a major stimulator of autoimmu-nity in rats with pristane-induced arthritis. J Immunol 179:7568–7576.CrossRefGoogle ScholarPubMed
Andersson, A.K., Li, C., and Brennan, F.M. 2008. Recent developments in the immunobiology of rheumatoid arthritis. Arthritis Res Ther 10(2):204. Epub March 14, 2008.CrossRefGoogle ScholarPubMed
Asquith, D.L., Miller, A.M., McInnes, I.B., and Liew, F.Y. 2009. Animal models of rheumatoid arthritis. Eur J Immunol. 39(8):2040–2044.CrossRefGoogle ScholarPubMed
Billingham, M.E.J. 1983. Models of arthritis and the search for anti-arthritic drugs. Pharmacol Ther 21:389–428.CrossRefGoogle ScholarPubMed
Hegen, M., Keith, J.C., Mary, C., and Nickerson-Nutter, C. 2008. Utility of animal models for identification of potential therapeutics for Rheumatoid Arthritis. Ann Rheum Dis 67:1505–1515.CrossRefGoogle ScholarPubMed
Henderson, B., Edwards, J.C.W., and Pettipher, E.R. (eds.) 1995. Mechanisms and Models in Rheumatoid Arthritis. London: Academic Press.
Joosten, L.A.B., and van den Berg, W. 2006. Murine collagen-induced arthritis. In: In Vivo Models of Inflammation. Progress in Inflammation Research. Parnham, M.J. (ed.), 2nd Ed., Vol 1, pp. 1–34. Basel: Birkhauser.Google Scholar
Kannan, K., Ortmann, R.A., and Kimpel, D. 2005. Animal Models of rheumatoid arthritis and their relevance to human disease. Pathophysiology 12:167–181.CrossRefGoogle ScholarPubMed
Paska, W., McDonald, K.J., and Crofy, M. 1986. Studies on type-II collagen induced arthritis in mice. Inflamm Res 18:413–420.Google ScholarPubMed
Rioja, I., Bush, K.A., Buckton, J.B., Dickson, M.C., and Life, P.F. 2004. Joint cytokine quantification in two rodent arthritis models: kinetics of expression, correlation of mRNA and protein levels and response to prednisolone treatment. Clin Exp Immunol 137:65–73.CrossRefGoogle ScholarPubMed
Schett, G., Stach, C., Zwerina, J., Voll, R., and Manger, B. 2008. How do anti-rheumatic drugs protect joints from damage in rheumatoid arthritis. Arthritis Rheum 58:2936–2948.CrossRefGoogle ScholarPubMed
Seed, M.P. 2009. Development of disease-modifying treatments for rheumatoid arthritis. Pharm J 282:191–192.Google Scholar
Seed, M.P., and Walsh, D. (eds.) Angiogenesis in Inflammation: Mechanisms and Clinical Correlates. Progress in Inflammation Research. Basel: Birkhauser.
Stevenson, C.S., Marshall, L.A., and Morgan, D.W. (Eds.) 2006. In Vivo Models of Inflammation, 2nd Ed., Vol 1. Progress in Inflammation Research. Basel: Birkhauser.CrossRef
Stevenson, C.S., Marshall, L.A., and Morgan, D.W. (Eds.) 2006. In Vivo Models of Inflammation, Vol 2. Progress in Inflammation Research. Basel: Birkhauser.CrossRef
Tak, P-P. (Ed.) 2009. New Therapeutic Targets in Rheumatoid Arthritis. Progress in Inflammation Research. Basel: Birkhauser.CrossRef
Van den Berg., W.B., and Miossec, P. (Eds.) 2004. Cytokines and Joint Injury. Progress in Inflammation Research. Basel: Birkhauser.CrossRef
Van den Berg, W., van Lent, P.L., Joosten, L.A., Abdollahi-Roodsaz, S., and Koenders, M.I. 2007. Amplifying elements of arthritis and joint destruction. Ann Rheum Dis 666(s3):iii45–iii48.Google Scholar
Wooley, P. 1991. Animal models of arthritis. Curr Opin Rheumatol 3:407–420.CrossRefGoogle ScholarPubMed
Wooley, P. 2008. Immunotherapy in collagen-induced arthritis: past, present, and future. Am J Med Sci. 327:217–226.Google Scholar

Save book to Kindle

To save this book to your Kindle, first ensure coreplatform@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×