Mechanism for nonspecific immunity of Listeria monocytogenes in rats mediated by platelets and the clotting system.

A proposed mechanism for nonspecific immunity to Listeria monocytogenes in rats based on the existence of an activatable lysin is described. Using a deoxyribonucleic acid release assay, we found lysin activity in serum made from whole blood but not in serum made from platelet-free plasma. Washed platelets and platelet lysates exhibited only partial activity as compared with that in serum. This activity was amplified by the addition of platelet-free plasma serum. The activity of the lysin was unaffected by heparin, dialysis, a serine esterase inhibitor, or heating to 56 degrees C for 30 min. Effective inhibitors were ethylenediaminetetraacetic acid and stronger heating (to 65 degrees C). Listeria organisms were found to reduce the recalcified clotting time to platelet-rich plasma in a dose-dependent fashion, indicating that the organisms can exhibit procoagulant activity. The susceptibility of rats to Listeria infection was enhanced by anticoagulant treatment. Rats were infected with Listeria organisms with and without administration of heparin. Heparin-treated rats developed bacteremia, and some died. None of the control rats developed bacteremia or died. These results suggest that natural immunity to Listeria infection is partly due to a platelet-dependent lysin which is activated during clotting and is, in turn, promoted by the Listeria organisms themselves.