Blockade of endogenous interleukin 12 results in suppression of murine streptococcal cell wall arthritis by enhancement of interleukin 10 and interleukin 1Ra

Article Abstract:

Blocking the activity of interleukin-12 may benefit arthritis patients. In a study of mice with experimentally induced arthritis, a chemical that blocks IL-12 reduced joint swelling. This shows that interleukin-12 stimulates inflammation.

Research, Inflammation, Inflammation mediators, Interleukin-12

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Chondrite IGF-1 receptor expression and responsiveness to IGF-1 stimulation in mouse articular cartilage during various phases of experimentally induced arthritis

Article Abstract:

Arthritis may impair the functioning of insulin like growth factor-1 (IGF-1) receptors. IGF-1 normally regulates protein production in healthy joint cartilage cells. Researchers measured the IGF-1 receptor expression in healthy mouse cartilage and the response to IGF-1 stimulation in arthritis-induced mouse cartilage. They found the majority of the IGF-1 receptors in the middle and deeper layers of the healthy mouse cartilage. Cartilage cells lost their capacity to respond to IGF-1, protein production decreased by 80%, and joint swelling was observed twelve hours after enzyme-induced arthritis. Four days later IGF-1 response, protein production, and joint inflammation returned to normal levels. They saw a similar response cycle with antigen-induced arthritis. However, IGF-1 response returned in 24 hours and protein production recovered in seven days with antigen-induced arthritis.

Rheumatoid arthritis, Insulin-like growth factors, Somatomedins, Articular cartilage

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Role of tumour necrosis factor alpha in experimental arthritis: separate activity of interleukin 1beta in chronicity and cartilage destruction

Article Abstract:

Drugs to treat arthritis would need to block the activity of both tumor necrosis factor and interleukin-1. These are proteins produced by the body that are involved in inflammatory processes. Both have been implicated in the development of arthritis.

Tumor necrosis factor, Interleukin-1

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