Tropomyosin-induced arthritis in rats

CER3090
2007 Vol.25, N°4 ,Suppl.45
PI 0086, PF 0092
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PMID: 17949558 [PubMed]

Abstract

OBJECTIVES:
Immunization of rats with α-tropomyosin (TPM) led to arthritis, uveitis and dermatitis, typical features of Behçet’s disease (BD). The present study characterizes the arthritic features of this animal model, not previously described.
METHODS:
Lewis rats were immunized with bovine α-TPM and another group of rats was treated with neutralizing anti- tumor necrosis factor-α (TNF-α) antibodies.
RESULTS:
Clinically more than 90% of the immunized rats developed severe acute arthritis 12 days after vaccination. Rats that were followed-up for 6 months had persistent inflammation of the leg joints. Histologic studies demonstrated predominant mononuclear infiltrations in the acute phase of arthritis; the chronic arthritic process resulted in cartilage and bone damage and abundant fibrosis which led to joint deformations. Male and female rats had a similar clinical course. Analysis of the splenocyte cytokine profile kinetics revealed a persistently high level of interferon-gamma (INF-&ggr;) and an increase in TNF-α secretion during the acute phase. Increasing levels of interleukin (IL)-10 heralded the decline in clinical arthritis. No IL-4 was detected. No arthritis was detected in the rats treated with anti-TNF-α antibodies.
CONCLUSIONS:
The data indicates that α-TPM serves as an autoantigen to induce acute and chronic destructive arthritis in rats. This model is a TNF-α dependent autoimmune disease, with a Th1 cytokine profile.