Resistance to Listeria monocytogenes (L.M.) in diabetic state was studied using streptozotocin (SZ)-induced diabetic mice. SZ-diabetic mice showed an enhanced resistance to primary listerial infection with a sublethal dose of inoculum, whereas there was no difference between normal and diabetic hosts when challenged with a lethal dose. The growth of L.M. in diabetic mice was inhibited at an early stage of infection. However viable Listeria survived in diabetic mice at a later stage, suggesting the trend of persisting infection. Such enhanced resistance to L.M. in diabetic mice was associated with increased rate of spreading of peritoneal macrophages and with reduction in the level of delayed type hypersensitivity (DTH) to L.M. Therefore, it seemed likely that the enhanced resistance to Listeria in diabetic mice would be due to nonspecifically activated macrophages. Secondary challenge in the immunized animals and transfer experiment with immune spleen cells revealed that the development of protective immunity in diabetic mice was inferior to that in normal mice. Treatment with insulin could hardly influence the altered resistance to L.M. in diabetic mice.