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The comparative study of Sprague–Dawley and Lewis rats in adjuvant-induced arthritis

  • X. Cai
  • Y. F. Wong
  • H. Zhou
  • Y. Xie
  • Z. Q. Liu
  • Z. H. Jiang
  • Z. X. Bian
  • H. X. Xu
  • L. LiuEmail author
Original Article

Abstract

The outbred Sprague–Dawley (SD) rats, similar to the inbred Lewis (LEW) rats, have been recently demonstrated to be highly susceptible to adjuvant-induced arthritis (AIA). We herein compared AIA in SD and LEW rats in terms of clinical, histological, radiological, and immuno-inflammatory features. The results showed that, following inoculation with a ground Mycobacterium tuberculosis (MT) suspension, SD and LEW rats manifested closely similar disease progression, with 100% incidence and similar severity. The development of arthritis was accompanied by significantly higher erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels than in control rats. Radiographic examination of the hind paws showed that both SD and LEW AIA rats manifested conspicuous soft tissue swelling, bone matrix resorption, periosteal new bone formation and bone erosion, while histopathological analysis of the synovial joints revealed marked cellular infiltration, angiogenesis, synovial hyperplasia, pannus formation, narrowing of joint space, and cartilage and bone destruction. Moreover, in relation to disease progression, serum tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 levels were markedly overexpressed in both SD and LEW AIA versus control rats, and SD and LEW AIA rats exhibited divergent profiles for the expression of TNF-α and IL-1β. Taken together, these results demonstrated that the SD rat AIA model shares several arthritic features with the comparable model in LEW rats. Hence, given the more favorable characteristics of SD rats than LEW rats (i.e., lower cost, wider availability, and heterogenic background), this SD rat AIA model is more cost effective and advantageous for screening and testing novel anti-arthritic agents.

Keywords

Adjuvant-induced arthritis Sprague–Dawley rats Lewis rats Mycobacterium tuberculosis Pro-inflammatory cytokines 

Notes

Acknowledgments

This research was funded by the Hong Kong Jockey Club Charities Trust. We are grateful to Profs. Biao Yan Du, Pei Xun Wang and Liang Zhou of the Guangzhou University of Traditional Chinese Medicine (GUTCM), for their assistance in histological analysis, and to Ms. Rui Yan Liang of GUTCM and Mr. Yong Huang and Mr. Yao Hua Huang of the First Affiliated Hospital of GUTCM for their assistance in radiographic analysis. We also thank Dr. Martha Dahlen for her excellent language editing of the manuscript.

References

  1. Anderson GD, Hauser SD, Mcgarity KL, Bremer ME, Isakson PC, Gregory SA (1996) Selective inhibition of cyclooxygenase (COX)-2 reverses inflammation and expression of COX-2 and interleukin 6 in rat adjuvant arthritis. J Clin Invest 97:2672–2679PubMedCrossRefGoogle Scholar
  2. Banik RK, Kasai M, Mizumura K (2002) Reexamination of the difference in susceptibility to adjuvant-induced arthritis among LEW/Crj, Slc/Wistar/ST and Slc/SD rats. Exp Anim 51:197–201PubMedCrossRefGoogle Scholar
  3. Billingham ME (1983) Models of arthritis and the search for anti-arthritic drugs. Pharmacol Ther 21:389–428PubMedCrossRefGoogle Scholar
  4. Bull BS, Caswell M, Ernst E, Kallner A, Koepke JA, Lewis SM, Lowe GDO, Rampling MW, Stuart J (1993) ICSH recommendations for measurement of erythrocyte sedimentation rate. J Clin Pathol 46:198–203CrossRefGoogle Scholar
  5. Burger D, Rezzonico R, Li JM, Modoux C, Pierce RA, Welgus HG, Dayer J (1998) Imbalance between interstitial collagenase and tissue inhibitor of metalloproteinases 1 in synoviocytes and fibroblasts upon direct contact with stimulated T lymphocytes: involvement of membrane-associated cytokines. Arthritis Rheum 41:1748–1759PubMedCrossRefGoogle Scholar
  6. Cai X, Zhou H, Wong YF, Xie Y, Liu ZQ, Jiang ZH, Bian ZX, Xu HX, Liu L (2005) Suppressive effects of QFGJS, a preparation from an anti-arthritic herbal formula, on rat experimental adjuvant-induced arthritis. Biochem Biophys Res Commun 337:586–594PubMedCrossRefGoogle Scholar
  7. Deodhar AA, Woolf AD (1996) Bone mass measurement and bone metabolism in rheumatoid arthritis: a review. Br J Rheumatol 35:309–322PubMedCrossRefGoogle Scholar
  8. Esser RE, Hildebrand AR, Angelo RA, Watts LM, Murphey MD, Baugh L (1995) Measurement of radiographic changes in adjuvant-induced arthritis in rats by quantitative image analysis. Arthritis Rheum 38:129–138PubMedCrossRefGoogle Scholar
  9. Feldmann M, Maini RN (2001) Anti-TNF alpha therapy of rheumatoid arthritis: what have we learned? Annu Rev Immunol 19:163–196PubMedCrossRefGoogle Scholar
  10. Feldmann M, Brennan FM, Maini RN (1996) Role of cytokines in rheumatoid arthritis. Annu Rev Immunol 14:397–440PubMedCrossRefGoogle Scholar
  11. Goldring SR (1996) Osteoporosis and rheumatic diseases. In: Favus MJ (ed) Primer on the metabolic bone diseases and disorders of mineral metabolism, 3rd edn. Lippincott-Raven, Philadelphia, pp 299–301Google Scholar
  12. Gravallese EM, Goldring SR (2000) Cellular mechanism and the role of cytokines in bone erosions in rheumatoid arthritis. Arthritis Rheum 43:2143–2151PubMedCrossRefGoogle Scholar
  13. Kushner I (1991) C-reactive protein in rheumatology. Arthritis Rheum 34:1065–1068PubMedCrossRefGoogle Scholar
  14. Maini RN, Taylor PC (2000) Anti-cytokines therapy for rheumatoid arthritis. Annu Rev Med 51:207–229PubMedCrossRefGoogle Scholar
  15. McCartney-Francis NL, Chan J, Wahl SM (2003) Inflammatory joint disease: clinical, histological, and molecular parameters of acute and chronic inflammation and tissue destruction. In: Winyard PG, Willoughby DA (eds) Inflammation protocols. Humana Press, New Jersey, pp 147–159CrossRefGoogle Scholar
  16. McGonagle D, Conaghan PG, O’Connor P, Gibbon W, Green M, Wakefield R, Ridgway J, Emery P (1999) The relationship between synovitis and bone changes in early untreated rheumatoid arthritis: a controlled magnetic resonance imaging study. Arthritis Rheum 42:1706–1711PubMedCrossRefGoogle Scholar
  17. Newbould BB (1964) Role of lymph nodes in adjuvant-induced arthritis in rats. Ann Rheum Dis 23:392–396PubMedCrossRefGoogle Scholar
  18. Panayi GS, Lanchbury JS, Kingsley GH (1992) The importance of the T cell in initiating and maintaining the chronic synovitis of rheumatoid arthritis. Arthritis Rheum 35:729–735PubMedCrossRefGoogle Scholar
  19. Pascual V, Allantaz F, Arce E, Punaro M, Banchereau J (2005) Role of interleukin-1 (IL-1) in the pathogenesis of systemic onset juvenile idiopathic arthritis and clinical response to IL-1 blockade. J Exp Med 201:1479–1486PubMedCrossRefGoogle Scholar
  20. Pearson CM (1956) Development of arthritis, periarthritis and periostitis in rats given adjuvant. Proc Soc Exp Biol Med 91:95–101PubMedGoogle Scholar
  21. Pearson CM (1963) Experimental joint disease observations on adjuvant-induced arthritis. J Chronic Dis 16:863–874PubMedCrossRefGoogle Scholar
  22. Pepys MB, Hirschfield GM (2003) C-reactive protein: a critical update. J Clin Invest 111:1805–1812PubMedGoogle Scholar
  23. Rosenthale ME (1970) A comparative study of the Lewis and Sprague Dawley rat in adjuvant arthritis. Arch Int Pharmacodyn Ther 188:14–22PubMedGoogle Scholar
  24. Smolen JS, Steiner G (2003) Therapeutic strategies for rheumatoid arthritis. Nat Rev Drug Discov 2:473–488PubMedCrossRefGoogle Scholar
  25. Szekanecz Z, Koch AE, Kunkel SL, Strieter RM (1998) Cytokines in rheumatoid arthritis: potential targets for pharmacological intervention. Drug Aging 12:377–390CrossRefGoogle Scholar
  26. van Eden W, Holoshitz J, Nevo Z, Frenkel A, Klajman A, Cohen IR (1985) Arthritis induced by a T-lymphocyte clone that responds to M. tuberculosis and to cartilage proteoglycans. Proc Natl Acad Sci U S A 82:5117–5120PubMedCrossRefGoogle Scholar
  27. van Eden W, Wagenaar-Hilbers JPA, Wauben MHM (1994) Animal models for autoimmune and inflammatory disease: adjuvant arthritis in the rat. In: Colagin JE (ed) Current protocols in immunology. Wiley, New York, pp 1–11Google Scholar
  28. van Leeuwen MA, van Rijswijk MH (1994) Acute phase proteins in the monitoring of inflammatory disorders. Baillieres Clin Rheumatol 8:531–552PubMedCrossRefGoogle Scholar
  29. van Vollenhoven RF, Thole JER, van der Zee R, Noordzij A, van Embden JDA, Hensen EJ, Cohen IR (1988) The role of immunity to cartilage proteoglycan in adjuvant arthritis: intravenous injection of bovine proteoglycan enhances adjuvant arthritis. J Immunol 141:1168–1173PubMedGoogle Scholar
  30. Waksman BH, Pearson CM, Sharp JT (1960) Studies of arthritis and other lesions induced in rats by injection of mycobacterial adjuvant. II. Evidence that the disease is a disseminated immunologic response to exogenous antigen. J Immunol 85:403–417PubMedGoogle Scholar
  31. Wolfe F, Michaud K (1994) The clinical and research significance of the erythrocyte sedimentation rate. J Rheumatol 21:1227–1237PubMedGoogle Scholar

Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  • X. Cai
    • 1
  • Y. F. Wong
    • 1
  • H. Zhou
    • 1
  • Y. Xie
    • 1
  • Z. Q. Liu
    • 1
  • Z. H. Jiang
    • 1
  • Z. X. Bian
    • 1
  • H. X. Xu
    • 2
  • L. Liu
    • 1
    Email author
  1. 1.School of Chinese MedicineHong Kong Baptist UniversityKowloonPeople’s Republic of China
  2. 2.Hong Kong Jockey Club Institute of Chinese Medicine LimitedKowloonPeople’s Republic of China

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