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五株小鼠感染伯氏疟原虫的免疫病理学方面。II. 感染期间脑及其他组织病变的免疫病理学

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

作者信息

Mackey L J, Hochmann A, June C H, Contreras C E, Lambert P H

出版信息

Clin Exp Immunol. 1980 Dec;42(3):412-20.

PMID:7011607
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1537166/
Abstract

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.

摘要

在A/J、BALB/c、OF1、CBA和C57B1小鼠中研究了伯氏疟原虫感染过程中的组织学变化。结合血清学方面的研究结果进行了分析(孔特雷拉斯等人,1980年)。A/J、BALB/c和OF1小鼠出现高死亡率和急性死亡,从第15天起在这些品系小鼠中发现明显的脑部病变,包括脑膜和脑静脉及毛细血管充血、大量被寄生红细胞阻塞这些血管、脑水肿和出血。此类病变在CBA和C57B1小鼠中极少,在感染后21天和24天检查的小鼠中未出现。从第9天起,通过免疫荧光在大多数小鼠的脉络丛中检测到IgG小沉积物和微量C3。肾脏病变包括充血、静脉和毛细血管堵塞、轻度单核细胞浸润和系膜增厚;这些变化在CBA、C57B1和A/J小鼠中最为明显。在感染的第一周,所有品系小鼠的肾小球均有IgM沉积物。在第二周检测到IgG和C3,但在CBA小鼠中仅发现微量。肝脏表现为充血、肿胀的库普弗细胞中色素积聚和单核细胞门静脉浸润;这些在A/J小鼠中最为明显。在脾脏中,网状内皮细胞数量大幅增加、白髓增殖、充血、色素积聚和浆细胞反应;不同品系小鼠白髓扩张的模式各不相同。结果表明,脑部病变在该疟疾模型急性死亡的病因学中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b49/1537166/81dc85c082f8/clinexpimmunol00189-0017-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b49/1537166/e0d7051da6e3/clinexpimmunol00189-0014-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b49/1537166/ab41068f68ce/clinexpimmunol00189-0015-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b49/1537166/2f1d57323457/clinexpimmunol00189-0016-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b49/1537166/81dc85c082f8/clinexpimmunol00189-0017-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b49/1537166/e0d7051da6e3/clinexpimmunol00189-0014-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b49/1537166/ab41068f68ce/clinexpimmunol00189-0015-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b49/1537166/2f1d57323457/clinexpimmunol00189-0016-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b49/1537166/81dc85c082f8/clinexpimmunol00189-0017-a.jpg

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