Modulation of cell recruitment by anti-inflammatory agents in antigen-induced arthritis. Issue 11 (1st November 2002)

• Record Type: Journal Article
• Authors: López-Armada, M J; Sánchez-Pernaute, O; Largo, R; Diez-Ortego, I; Palacios, I; Egido, J; Herrero-Beaumont, G
• Is Part Of: Annals of the rheumatic diseases. Volume 61:Issue 11(2002)
• Page Start: 1027
• Page End: 1030
• Publication Date: 2002-11-01
• Subjects: chemokines -- cyclo-oxygenase -- prostaglandin E2 -- arthritis; COX, cyclo-oxygenase -- DCF, diclofenac -- IL, interleukin -- MCP-1, monocyte chemotactic peptide-1 -- MN, mononuclear cells -- MXC, meloxicam -- NSAIDs, non-steroidal anti-inflammatory drugs -- PGE2 -- prostaglandin E2 -- PMN, polymorphonuclear cells -- SF, synovial fluid -- SM, synovial membrane; Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/ard.61.11.1027
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Objective: To study the effect of meloxicam (MXC) and diclofenac (DCF) on the recruitment of leucocytes during acute experimental arthritis. Methods: Rabbits with antigen-induced arthritis were treated with MXC, DCF, or not treated. After 48 hours, synovial fluid (SF) leucocyte influx and prostaglandin E2 (PGE2 ) levels were evaluated. Interleukin 8 (IL8) and monocyte chemotactic peptide-1 (MCP-1) expression and synthesis were studied in the inflamed tissues. Results: Arthritic knees showed synovial effusion with a high leucocyte count and PGE2 concentration, and an increased expression of IL8 and MCP-1. Both non-steroidal anti-inflammatory drugs (NSAIDs) reduced PGE2 levels and the polymorphonuclear cell (PMN) concentration in SF, while the mononuclear cell (MN) concentration was unchanged in the treated groups in comparison with controls. A definite reduction of IL8 levels was obtained with the treatments, but the drugs did not prevent the up regulation of MCP-1. Conclusion: The effect of these NSAIDs in acute arthritis may be related to the down regulation of IL8 production. The results suggest a differential effect of anti-inflammatory drugs on PMN and MN recruitment to the joint.