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American Journal of Pathology, Vol 137, 1077-1082, Copyright © 1990 by American Society for Investigative Pathology

REGULAR ARTICLES

Pathogenesis of antigen-induced arthritis in mice deficient in neutrophil elastase and cathepsin G

R Pettipher, J Edwards, S Cruwys, E Jessup, J Beesley and B Henderson
Department of Pharmacology, Wellcome Research Laboratories, Beckenham, Kent, United Kingdom.

The contribution of neutrophil-derived elastase and cathepsin G to joint pathology has been examined in immune arthritis in the mouse. Neutrophils from beige mice are genetically deficient in lysosomal elastase and cathepsin G, but have normal levels of the acid hydrolases, beta-glucuronidase, and N-acetyl-beta-glucosaminidase. The development of antigen-induced arthritis in normal mice has been compared with that in beige mice. The pattern of synovitis (both leukocyte accumulation and plasma leakage) were indistinguishable in normal and beige mice. Cartilage proteoglycan depletion was quantified by measuring the decrease in safranin O staining intensity, and this, too, was unaltered in mice lacking elastase and cathepsin G. These results suggest that neutrophil elastase and cathepsin G do not contribute to these aspects of joint pathology in antigen-induced arthritis in the mouse.


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