Lysozyme and β-Lysin Release Stimulated by Antigen-Antibody Complexes and Bacteria

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Abstract
Summary: The concentrations of plasma lysozyme and β-lysin increased several-fold following the intravenous injection of either dead bacteria or antigen-antibody complexes into normal rabbits, or of BSA into immunized rabbits. Histamine and serotonin were not responsible for these alterations. The exposure of whole blood to dead Micrococcus lysodeikticus in vitro also resulted in a significant release of β-lysin and lysozyme into plasma. Similar exposures of peritoneal phagocytes to antigen-antibody complexes or bacteria resulted in the release of lysozyme during phagocytosis. Exposure of β-lysin-rich platelets to either antigen-antibody complexes or micrococci in vitro did not cause a consistent release of β-lysin. The in vivo release of β-lysin was accompanied by a decrease in the number of circulating platelets, a decrease in β-lysin per unit platelet, and extensive morphologic damage of platelets. For these reasons the in vivo results could be attributed to the release of β-lysin from platelets.

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