The effect of leukocyte hydrolases on bacteria : V. Modification of bacteriolysis by antiinflammatory agents and by cationic and anionic polyelectrolytes

Abstract

Lysis of(14)C-labeledStaph. aureus by human blood leukocyte lysates, by extracts of rabbit small intestines and pancreas, and by the "cocktail" of enzymes (containing trypsin, lysolecithin, and lysozyme) is strongly inhibited by anionic polyelectrolytes (e.g., heparin, chondroitin sulfate, liquoid (polyanethole sulfonic acid), and DNA). Most of the lytic agents employed were inhibited by cationic polyelectrolytes (e.g., histone, protamin sulfate and polylysin), as well as by gold thiomalate, normal human serum, synovial fluids obtained from patients with knee-joint trauma, extracts of coffee, tea, and cocoa, Ultracorten- and Dexamethasone. On the other hand, some antiinflammatory agents tested (e.g., indomethacin, aspirin, hydrocortisone acetate and succinate, and prednisolone acetate and tributyl acetate) were not inhibitory. All the cationic polyelectrolytes employed and liquoid were also strong inhibitors of lysozyme. Since mixtures of cationic and anionic polyelectrolytes at equimolar concentrations failed to inhibit bacteriolysis, it is postulated that the balance between charged macromolecular substances, which are likely to accumulate in inflammatory foci, may determine the fate of cellular components of bacteria in inflamed tissues. The possible role played by lysosomal enzymes and by tissue inhibitors in tissue damage and in the survival of bacteria in chronic inflammatory lesions is discussed.