Ishibashi T, Kitahara Y, Kaziki A, Harada Y, Takamoto M, Ishibashi T
Jpn J Exp Med. 1981 Oct;51(5):251-9.
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.
利用链脲佐菌素（SZ）诱导的糖尿病小鼠研究了糖尿病状态下对单核细胞增生李斯特菌（L.M.）的抵抗力。SZ诱导的糖尿病小鼠对亚致死剂量接种物的原发性李斯特菌感染表现出增强的抵抗力，而当用致死剂量攻击时，正常宿主和糖尿病宿主之间没有差异。L.M.在糖尿病小鼠体内的生长在感染早期受到抑制。然而，在感染后期，活的李斯特菌在糖尿病小鼠体内存活下来，表明存在持续感染的趋势。糖尿病小鼠对L.M.的这种增强抵抗力与腹膜巨噬细胞扩散率增加以及对L.M.的迟发型超敏反应（DTH）水平降低有关。因此，糖尿病小鼠对李斯特菌的抵抗力增强似乎是由于非特异性激活的巨噬细胞。对免疫动物的二次攻击和用免疫脾细胞进行的转移实验表明，糖尿病小鼠中保护性免疫的发展不如正常小鼠。胰岛素治疗几乎不能影响糖尿病小鼠对L.M.抵抗力的改变。
