Progression of Articular Destruction and the Production of Tumour Necrosis Factor‐α in Antigen‐Induced Arthritis in Rabbits

Abstract

Idogawa H, Imamura A, Onda M, Umemura T, Ohashi M. Progression of Articular Destruction and the Production of Tumour Necrosis Factor-a in Antigen-Induced Arthritis in Rabbits. Scand J Immunol 1997; 46:572-580 We examined the progression of articular destruction and the production of tumour necrosis factor-a (TNF-a) in antigen-induced arthritis (AIA) in rabbits, i.e. flare-ups of inflammation induced by repeated intra-articular injections (single, twice and three times) of antigen. A marked progression of articular destruction and an infiltration of inflammatory cells in the synovium were observed with the increase in the number of antigen injections. An immunohistochemical analysis of the synovial lesions following three injections of antigen revealed that the lymphoid follicles consisted mainly of CD4 þ T cells and IgG/IgM þ B cells. There were marked infiltrations of IgG þ plasma cells around the lymphoid follicles. In contrast, the production of TNF-a in the synovial fluid and the erythrocyte sedimentation rate (ESR), which is a marker of systemic inflammatory activity in rheumatoid arthritis, peaked at 6 h and 24 h, respectively, following the last injection of antigen. These values were also greater following the repeated injections of antigen compared with the single injection. The TNF-a was produced markedly in the joints at the onset of the flare-ups of arthritis following the repeated injections of antigen, and the elevation of the ESR and an acceleration of the inflammatory response in the synovium were observed with a concomitant progression of severe articular destruction, suggesting that the marked production of TNF-a at the time of flare-ups may be involved in the exacerbation of AIA in rabbits.

Modulation of fibroblast-mediated cartilage degradation by articular chondrocytes in rheumatoid arthritis

“…Interestingly, addition of human TNF␣ did not enhance the degradation of the cartilage-like matrix. Although it has been shown convincingly that high concentrations of TNF␣ may enhance the destructive potential of FLS (18)(19)(20), our data confirm recent observations suggesting a role of TNF␣ primarily in synovial inflammation (21).…”

Association between condylar morphology and changes in bony microstructure and sub-synovial inflammation in experimental temporomandibular joint arthritis

“…These changes were seen at the macro-morphological level and only very few differences were seen at the micro-architectural level, indicating growth disturbances rather than bone destruction. The antigen-induced TMJ arthritis model has been shown to be both IL-1 and TNF-a driven in the acute stages of inflammation (14)(15)(16)(17). In rabbits treatment of antigen-induced arthritis in the knee with monoclonal anti-TNF therapy resulted in reduced inflammation (17).…”

“…The antigen‐induced TMJ arthritis model has been shown to be both IL‐1 and TNF‐α driven in the acute stages of inflammation (14–17). In rabbits treatment of antigen‐induced arthritis in the knee with monoclonal anti‐TNF therapy resulted in reduced inflammation (17).…”

Blocking of Interleukin-17 during Reactivation of Experimental Arthritis Prevents Joint Inflammation and Bone Erosion by Decreasing RANKL and Interleukin-1

“…4 Studies in animal models for experimental arthritis have resulted in better understanding of the role of different cell types and various cytokines during arthritic flares. In antigen-induced arthritis, the capacity to develop arthritis can be transferred by lymphocytes, 6 in particular by cell fractions enriched for T cells, and high numbers of T cells can be detected in the inflamed synovium after flare-up reaction. 7 Reactivation of chronic streptococcal cell wall arthritis in Lewis rats could be prevented by removal of T lymphocytes, 8 and successful suppression of antigen-induced arthritis (AIA)-flare in mice treated with anti-lymphocyte serum 9 or anti-CD4 monoclonal antibodies 10 also suggests an important role for T cells in this process.…”