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IL‐1β and TNF‐α Produce Divergent Acute Inflammatory and Skeletal Lesions in the Knees of Lewis Rats

Arthritis is initiated and sustained by the release of myriad pro-inflammatory cytokines.1 In patients with rheumatoid arthritis, the dominant pro-inflammatory cytokines are interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α).2 Inhibition of IL-1β and/or TNF-α reduces the extent of inflammation in rheumatoid arthritis3,4 and in animal models of arthritis.5–7 Therefore, biologic agents that inhibit the action of these two cytokines are gaining rapid acceptance as early, aggressive treatments for rheumatoid arthritis. IL-1β and TNF-α act synergistically to induce and maintain inflammation and skeletal erosion in arthritis.1 The present study was designed to explore the early effects (48 h) by direct intra-articular injection of IL-1β or TNF-α. Our data show that both cytokines can initiate disease, but that IL-1β appears to play a more substantial role than TNF-α in the early stages of arthritis, particularly with respect to the induction of osseous lesions.