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Inhibition of Septic Arthritis by Local Administration of Taurine Chloramine, a Product of Activated Neutrophils
MARGARETA VERDRENGH and ANDREJ TARKOWSKI
ABSTRACT. Methods. The murine model of hematogenous septic arthritis involved intravenous injection of a single dose of Staphylococcus aureus. Tau-Cl was administered by daily intraperitoneal injections. In another experiment S. aureus and Tau-Cl were injected intra-articularly. Evaluation of arthritis was performed clinically and histologically. The effect of Tau-Cl on bacterial growth in vitro was also assessed. Results. Growth of staphylococci, including the methicillin-resistant strain 67-0, was inhibited by Tau-Cl. Mice injected with bacteria and Tau-Cl locally in the joint exhibited significantly fewer arthritic lesions. In contrast, there were no obvious differences between Tau-Cl-treated animals and controls with regard to clinical or histological signs of arthritis when bacteria and Tau-Cl were administered systemically. Conclusion. Our results show that Tau-Cl exerts an inhibitory effect on the development of bone and cartilage damage in the infected joint when administered intra-articularly. (J Rheumatol 2005; 32:1513-7) Key Indexing Terms:
TAURINE CHLORAMINE
From the Department of Rheumatology and Inflammation Research, Göteborg University, Göteborg, Sweden. Supported by grants from the Göteborg Medical Society, the Swedish Association against Rheumatism, the King Gustaf V Foundation, the Swedish Medical Research Council, the Nanna Svartz Foundation, the University of Göteborg, the A-G Crafoord Foundation, Börje Dahlin Foundation, the Inflammation Network, the Infection and Vaccination Network, the A. M. E. Wolff Foundation, Commission of the European Communities, specific RTD program "Quality of Life and Management of Staphylococcal Diseases (Antistaph)," and the Göteborg Association against Rheumatism. M. Verdrengh, PhD; A. Tarkowski, MD, Professor, Department of Rheumatology and Inflammation Research, Göteborg University. Address reprint requests to Dr. M. Verdrengh, Department of Rheumatology and Inflammation Research, Göteborg University, Guldhedsgatan 10A, SE-413 46 Göteborg, Sweden. E-mail: margareta.verdrengh@rheuma.gu.se Accepted for publication March 9, 2005. |