Inhibition of equine complement activity by polysulfated glycosaminoglycans

A. M. Rashmir-Raven From the Departments of Clinical Sciences (Rashmir-Raven, Coyne, Gaughan, DeBowes) and Pathology (Fenwick, Andrews), College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506.

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C. P. Coyne From the Departments of Clinical Sciences (Rashmir-Raven, Coyne, Gaughan, DeBowes) and Pathology (Fenwick, Andrews), College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506.

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B. W. Fenwick From the Departments of Clinical Sciences (Rashmir-Raven, Coyne, Gaughan, DeBowes) and Pathology (Fenwick, Andrews), College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506.

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E. M. Gaughan From the Departments of Clinical Sciences (Rashmir-Raven, Coyne, Gaughan, DeBowes) and Pathology (Fenwick, Andrews), College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506.

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G. A. Andrews From the Departments of Clinical Sciences (Rashmir-Raven, Coyne, Gaughan, DeBowes) and Pathology (Fenwick, Andrews), College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506.

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R. M. DeBowes From the Departments of Clinical Sciences (Rashmir-Raven, Coyne, Gaughan, DeBowes) and Pathology (Fenwick, Andrews), College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506.

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Summary

The ability of polysulfated glycosaminoglycans (psgag) to inhibit the complement cascade was evaluated. The role of complement in inflammation and infection has been well documented. Inhibition of the complement cascade by psgag could explain why intra-articularly administered psgag diminish diarthrodial joint inflammation and potentiate septic arthritis in horses.

Hemolytic complement testing was performed to evaluate the effect of psgag on the equine classical and alternate pathways of complement, using rabbit erythrocytes as the target cells. Concentration of psgag between 0.2 mg/ml and 0.6 mg/ml significantly (P< 0.05) inhibited equine complement in dose-related fashion. Further increase in complement inhibition was not observed at psgag concentration >0.6 mg/ml. Difference was not apparent in the extent of inhibition of complement from each of the 4 horses tested. Polysulfated glycosaminoglycans appeared to inhibit the classical and alternate complement pathways equally, indicating possible effect on complement components common to both pathways. Heat inactivation of complement function completely inhibited (P<0.01) the hemolytic activity of the serum from all horses.

Summary

The ability of polysulfated glycosaminoglycans (psgag) to inhibit the complement cascade was evaluated. The role of complement in inflammation and infection has been well documented. Inhibition of the complement cascade by psgag could explain why intra-articularly administered psgag diminish diarthrodial joint inflammation and potentiate septic arthritis in horses.

Hemolytic complement testing was performed to evaluate the effect of psgag on the equine classical and alternate pathways of complement, using rabbit erythrocytes as the target cells. Concentration of psgag between 0.2 mg/ml and 0.6 mg/ml significantly (P< 0.05) inhibited equine complement in dose-related fashion. Further increase in complement inhibition was not observed at psgag concentration >0.6 mg/ml. Difference was not apparent in the extent of inhibition of complement from each of the 4 horses tested. Polysulfated glycosaminoglycans appeared to inhibit the classical and alternate complement pathways equally, indicating possible effect on complement components common to both pathways. Heat inactivation of complement function completely inhibited (P<0.01) the hemolytic activity of the serum from all horses.

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