Immunopathological aspects of Plasmodium berghei infection in five strains of mice. II. Immunopathology of cerebral and other tissue lesions during the infection.

Immunopathological aspects of Plasmodium berghei infection in five strains of mice. II. Immunopathology of cerebral and other tissue lesions during the infection.
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五种小鼠品系中伯氏疟原虫感染的免疫病理学方面。

DOI:
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发表时间:
1980
影响因子:
4.6
通讯作者:
P. Lambert
P. Lambert
中科院分区:
医学3区
文献类型:
--
作者:
L. Mackey;A. Hochmann;C. June;C. Contreras;P. Lambert

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观察了A/J、BALB/c、OF 1、CBA和C57 B1小鼠感染伯氏疟原虫过程中的组织学变化。研究了与血清学方面相关的发现(Contreras等人,1980年)。在A/J、BALB/c和OF 1小鼠中发生高死亡率和急性死亡,并且从第15天开始在这些品系中发现明显的脑损伤,包括脑膜和脑静脉和毛细血管充血,这些血管被严重寄生的RBC阻塞,脑水肿和出血。这种病变在CBA和C57 B1小鼠中最小,在感染后21天和24天检查的小鼠中不存在。从第9天起,通过免疫荧光法在大多数小鼠的脉络丛中检测到IgG和微量C3的小沉积物。肾脏病变包括充血、静脉和毛细血管堵塞、低度单核细胞浸润和系膜增厚;这些变化在CBA、C57 B1和A/J小鼠中最为显著。在感染的第一周,所有菌株均存在IgM的肾小球沉积。在第二周检测到IgG和C3,但仅在CBA小鼠中发现痕量。肝脏显示充血、肿胀枯否细胞中色素蓄积和单核门静脉浸润;这些在A/J小鼠中最为明显。在脾脏中,网状内皮细胞群、白色髓增殖、充血和色素积累以及浆细胞反应大量增加;不同品系的白色髓扩张模式不同。结果表明,脑病变在该疟疾模型中急性死亡的病因学中起重要作用。
Histological changes during the course of P. berghei infection were investigated in A/J, BALB/c, OF1, CBA and C57B1 mice. The findings were studied in relation to serological aspects (Contreras et al., 1980). High mortality and acute deaths occurred in A/J, BALB/c and OF1 mice and marked cerebral lesions were found in these strains from day 15, including congestion of meningeal and cerebral veins and capillaries, blocking of these vessels by heavily parasitized RBC, cerebral oedema and haemorrhages. Such lesions were minimal in CBA and C57B1 mice, and absent in mice examined 21 and 24 days after infection. Small deposits of IgG and traces of C3 were detected by immunofluorescence in the choroid plexus of most mice from day 9. Renal lesions included congestion, plugging of veins and capillaries, low-grade mononuclear infiltration and mesangial thickening; these changes were most marked in CBA, C57B1 and A/J mice. Glomerular deposits of IgM were present in all strains in the first week of infection. IgG and C3 were detected in the second week, but only traces were found in CBA mice. The livers showed congestion, accumulation of pigment in swollen Kupffer cells and mononuclear portal infiltration; these were most pronounced in A/J mice. In the spleen, there was a great increase in the reticuloendothelial cell population, white pulp proliferation, congestion and accumulation of pigment and plasma cell reaction; the pattern of white pulp expansion varied in the different strains. The results suggest that cerebral lesions play a significant role in the aetiology of acute deaths in this malaria model.