Measurement of the chemotactic complement fragment C5a in rheumatoid synovial fluids by radioimmunoassay: role of C5a in the acute inflammatory phase

Article Abstract:

Besides chronic synovitis, or inflammation of the synovial tissue, which lines the joints, rheumatoid arthritis (RA) is characterized by acute exacerbations. It is important to determine the mechanisms contributing to these flare-ups, since they could eventually be modulated by drugs. Flare-ups have so far been found to consist of leakage of plasma proteins from blood vessels and movement of neutrophils, white blood cells that secrete cell-damaging products, into tissues. Studies have suggested that the complement system is activated in RA; this system consists of a group of proteins in the blood which, when sensitized, destroy bacteria and other cells. C5a is a product of complement activation which causes movement of neutrophils and other white blood cells, edema (fluid accumulation) and leakage of plasma proteins, and histamine release. Using a newly developed sensitive assay (test) for C5a, the levels of C5a in synovial fluid from 22 patients with RA (20 female) and 16 patients with other types of arthritis were measured. Blood levels of C5a were tested in 11 patients with RA, and were below the limits of the assay. In contrast, C5a levels synovial fluid from patients with RA were measurable and at levels which in the laboratory are capable of promoting neutrophil movement and accumulation, edema, and histamine release. Patients with systemic lupus erythematosus, osteoarthritis, or Reiter's disease also had increased C5a levels in synovial fluid, while those who had mechanically damaged joints had low C5a levels. High levels of another complement protein, C3a, were also found, though the levels correlated only slightly with those of C5a. However, C3a can only mediate histamine release but not neutrophil accumulation and edema. The study supports a role for C5a in mediating neutrophil accumulation leading to acute joint swelling in patients with rheumatoid arthritis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement

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Complement C1s activation in degenerating articular cartilage of rheumatoid arthritis patients: immunohistochemical studies with an active form specific antibody

Article Abstract:

The complement component C1s may participate in the dissolution of collagen and the cartilage degradation of rheumatoid arthritis. Complement components contribute to immunity by destroying invading cells and materials, such as pathogenic bacteria. Researchers tested cartilage samples from rheumatoid arthritic joints, osteoarthritic joints, and healthy joints. C1s was clearly present and active in joints from patients with rheumatoid arthritis, an autoimmune joint disease. C1s was less apparent, and not activated, in joints with osteoarthritis, and not present in healthy joint cartilage.

Japan, Cartilage

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Anti-tumour necrosis factor specific antibody (infliximab) treatment provides insights into the pathophysiology of rheumatoid arthritis

Article Abstract:

Blocking the activity of tumor necrosis factor (TNF) using a monoclonal antibody shows that TNF regulates the production of pro-inflammatory proteins, induces cell adhesion and cell migration into joints, and causes the formation of new blood vessels. TNF has been implicated in the development of rheumatoid arthritis.

Inflammation, Inflammation mediators, Tumor necrosis factor

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