Pathogenic responses of bradykinin system in chronic inflammatory rheumatoid disease.

摘要: Summary Excessive release of kinin (BK) in the synovial fluid can produce oedema, pain and loss functions due to activation B1 B2 receptors. Activation forming system could be mediated via injury, trauma, coagulation pathways (Hageman factor thrombin) immune complexes. The activated receptors might cause other powerful non-cytokine cytokine mediators inflammation, e.g., PGE2, PGI2, LTs, histamine, PAF, IL-1 TNF, derived mainly from polymorphonuclear leukocytes, macrophages, endothelial cells tissue. These are capable inducing bone cartilage damage, hypertrophic synovitis, vessel proliferation, inflammatory cell migration and, possibly, angiogenesis pannus formation. pathological changes, however, not yet defined human model chronic inflammation. role kinins their interacting would soon start clarify detailed questions they revealed clinical experimental models diseases. Several receptor antagonists being synthesized an attempt study molecular processes, such as rheumatoid arthritis, periodontitis, diseases gut osteomyelitis. Future development specific potent stable or combined with y-IFN serve a pharmacological basis for more effective treatment joint related