The neutrophil in rheumatoid arthritis: its role and the inhibition of its activation by nonsteroidal antiinflammatory drugs.
The activation of the polymorphonuclear leukocyte (PMN) in rheumatoid arthritis produces toxic products that include lysosomal enzymes, stable prostaglandins, and leukotrienes and causes the release of superoxide anion. These products produce the inflammatory response, damage cell membranes, and degrade hyaluronic acid. The inhibition of prostaglandin synthetase by NSAIDs does not, by itself, account for their effectiveness in preventing inflammation in rheumatoid arthritis. In vivo and in vitro experiments were conducted to determine if NSAIDs also exert an effect on neutrophil activation. The NSAIDs tested inhibited discrete PMN functions dependent upon the stimulus tested. The antiinflammatory effects of NSAIDs cannot be entirely explained by their inhibition of prostaglandin synthetase and may, in part, be due to other direct effects upon inflammatory cell activation.
D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001172:Arthritis, Rheumatoid / Q000378:metabolism*; D002449:Cell Aggregation / Q000187:drug effects; D002478:Cells, Cultured; D016861:Cyclooxygenase Inhibitors; D006801:Humans; D008855:Microscopy, Electron, Scanning; D009504:Neutrophils / Q000378:metabolism* / Q000648:ultrastructure; D010894:Piroxicam; D013481:Superoxides / Q000378:metabolism; D013843:Thiazines / Q000494:pharmacology
D000893:Anti-Inflammatory Agents; D016861:Cyclooxygenase Inhibitors; D013843:Thiazines; D013481:Superoxides; D010894:Piroxicam