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首页> 外文期刊>Infection and immunity >Enhanced susceptibility of mice with streptozotocin-induced diabetes to type II group B streptococcal infection.
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Enhanced susceptibility of mice with streptozotocin-induced diabetes to type II group B streptococcal infection.

机译：链脲佐菌素诱导的糖尿病小鼠对II型B组链球菌感染的敏感性增强。

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Since diabetes mellitus predisposes adults to group B streptococcal (GBS) bacteremia, a murine model of streptozotocin-induced diabetes and type II GBS bacteremia was developed to assess certain immune factors which might influence susceptibility to infection. In diabetic mice, the 50% lethal dose for two strains of type II GBS was significantly lower (greater than 1 log10 decrease in CFU per milliliter) than in control animals. This enhanced virulence of GBS for diabetic animals was associated with prolonged bacteremia, persistent sequestration of organisms in the splanchnic reticuloendothelial system, and a shift from splenic to hepatic clearance. Although immunization of control and diabetic animals resulted in high concentrations of type-specific serum antibody, it had no effect on late reticuloendothelial system sequestration in diabetics. In contrast, depletion of complement by treatment of mice with cobra venom factor blocked reticuloendothelial system clearance and resulted in fatal infection in both diabetic and control mice. These results indicate that neither type-specific antibody nor an intact complement system is adequate for effective clearance of type II GBS bacteremia in mice with experimentally induced diabetes. This clearance deficit could be the result of a defect in hepatocyte membrane receptors necessary for removal of this encapsulated microorganism.
机译：由于糖尿病使成年人更易患B群链球菌（GBS）菌血症，因此开发了一种由链脲佐菌素诱发的糖尿病和II型GBS菌血症的小鼠模型，以评估可能影响感染易感性的某些免疫因素。在糖尿病小鼠中，两种II型GBS菌株的50％致死剂量显着低于对照动物（CFU每毫升降低大于1 log10）。糖尿病动物对GBS的这种增强毒力与长时间的菌血症，内脏网状内皮系统中生物的持续隔离以及从脾脏清除到肝清除有关。尽管对对照动物和糖尿病动物进行免疫接种会导致高浓度的类型特异性血清抗体，但它对糖尿病患者后期网状内皮系统隔离没有影响。相反，用眼镜蛇毒因子治疗小鼠耗竭补体会阻断网状内皮系统清除，并在糖尿病和对照小鼠中导致致命性感染。这些结果表明，在实验诱发的糖尿病小鼠中，类型特异性抗体或完整的补体系统都不足以有效清除II型GBS菌血症。这种清除缺陷可能是去除这种被包封的微生物所必需的肝细胞膜受体缺陷的结果。

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