A method of experimental rheumatoid arthritis induction using collagen type II isolated from chicken sternal cartilage

Su,Zhaoliang; Shotorbani,Siamak   Sandoghchian; Jiang,Xugan; Ma,Rui; Shen,Huiling; Kong,Fanzhi; Xu,Huaxi

doi:10.3892/mmr.2013.1476

A method of experimental rheumatoid arthritis induction using collagen type II isolated from chicken sternal cartilage

Authors:
- Zhaoliang Su
- Siamak Sandoghchian Shotorbani
- Xugan Jiang
- Rui Ma
- Huiling Shen
- Fanzhi Kong
- Huaxi Xu
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Affiliations: Department of Immunology and Laboratory Immunology, Jiangsu University, Zhenjiang 212013, P.R. China, The Affiliated People's Hospital of Jiangsu University, Zhenjiang 212008, P.R. China
Published online on: May 14, 2013 https://doi.org/10.3892/mmr.2013.1476
Pages: 113-117

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Abstract

At present, collagen‑induced arthritis (CIA) is the best known and most extensively used model for the immunological and pathological characteristics of human rheumatoid arthritis (RA). This model is useful not only in aiding our understanding of the pathogenesis of this disease, but also in the development of new therapies. Bovine, porcine and human collagen has been used to induce CIA; however, response has been identified to vary between strains and injection conditions, and false positive results and reduced potency are common as a result of minor contaminants or deglycosylated protein. Therefore, in the present study, type II collagen (CII) was isolated and purified from chicken sternal cartilage and was found to successfully induce the RA model. Furthermore, T helper 17 (Th17) cells were observed to infiltrate the joint on day 45 following induction by CII. In vitro, expression of toll‑like receptor 2 (TLR2) increased in peritoneal macrophages stimulated by CII. In addition, blockage of TLR2 was identified to markedly decrease levels of TGF‑β and IL‑6 in the cell culture supernatant. The results indicate that CII isolated from chicken sternal cartilage may be recognized by TLR2 on macrophages, leading to TGF‑β and IL‑6 production and subsequent activation of Th17 cells which mediates CIA development.

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