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小鼠对福氏耐格里阿米巴感染的宿主抵抗力。

Host resistance of mice to Naegleria fowleri infections.

作者信息

Reilly M F, White K L, Bradley S G

出版信息

Infect Immun. 1983 Nov;42(2):645-52. doi: 10.1128/iai.42.2.645-652.1983.

Abstract

Naegleria fowleri is an etiological agent of primary amoebic meningoencephalitis in humans and laboratory animals. The determinative factors in host resistance of mice to N. fowleri infections have not been fully characterized. Male or female B6C3F1 mice stimulated by intraperitoneal administration of 10(6) amoebae of N. fowleri nN68 per mouse produced agglutinating activity and markedly elevated levels of serum and immunoglobulins M and G. Despite a marked humoral response, protective immunity was increased only marginally by active immunization. Host resistance was not impaired by prior treatment with 350 rads of 60Co radiation or 200 mg of cyclophosphamide per kg or by concurrent daily treatment with 30 mg of cyclophosphamide per kg for 14 days. Moreover, host resistance was not impaired by daily treatment with 4 mg of diethylstilbestrol per kg for 14 days, with challenge on day 2 of drug exposure or 24 h after the last drug treatment. Mice depleted of hemolytic complement by cobra venom factor were more susceptible to N. fowleri infection than were untreated mice.

摘要

福氏耐格里阿米巴是人类和实验动物原发性阿米巴脑膜脑炎的病原体。小鼠对福氏耐格里阿米巴感染的宿主抵抗力的决定性因素尚未完全明确。通过腹腔注射每只小鼠10(6)个福氏耐格里阿米巴nN68刺激的雄性或雌性B6C3F1小鼠产生了凝集活性,血清以及免疫球蛋白M和G水平显著升高。尽管有明显的体液反应,但主动免疫仅使保护性免疫略有增加。预先用350拉德的60Co辐射或每千克200毫克环磷酰胺处理,或同时每天用每千克30毫克环磷酰胺处理14天,宿主抵抗力并未受损。此外,每天用每千克4毫克己烯雌酚处理14天,在药物暴露第2天或最后一次药物治疗后24小时进行攻击,宿主抵抗力也未受损。用眼镜蛇毒因子耗尽溶血补体的小鼠比未处理的小鼠更容易受到福氏耐格里阿米巴感染。

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