Collagen-Induced Arthritis (CIA) Models

Charles River conducts contract studies in established mouse and rat models of collagen-induced arthritis (CIA) to explore disease pathogenesis and validate therapeutic targets. Susceptibility to collagen-induced rheumatoid arthritis is strongly associated with major histocompatibility complex class II genes, and the development of the disease is accompanied by a robust T-cell and B-cell inflammation response to type II collagen.

The chief pathological features of collagen-induced arthritis include a proliferative synovitis with infiltration of polymorphonuclear and mononuclear cells, pannus formation, cartilage degradation, erosion of bone and fibrosis. As in human rheumatoid arthritis, pro-inflammatory cytokines (e.g., TNF-a, IL-1b and IL-6) are increased in collagen-induced arthritis. Biological therapies designed to interfere with these mediators are active in these models.

Disease activity is determined by measuring inflammation swelling in the affected joints (paw volume or thickness) over time. Treatments can be assessed in either prophylactic or therapeutic testing paradigms. Additional measures of disease activity include evaluation of C-reactive protein (CRP) and erythrocyte sedimentation rate.

49-day study carried out in DBA1 mice using bovine or chicken type II collagen as an immunogen. Disease onset can be synchronized with LPS challenge.

28-day study carried out in Dark Agouti or Lewis rats using bovine or porcine type II collagen as an immunogen.

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