Neill A L, Chan-Ling T, Hunt N H
Department of Pathology, University of Sydney, N.S.W., Australia.
Parasitology. 1993 Dec;107 ( Pt 5):477-87. doi: 10.1017/s0031182000068050.
CBA/T6 mice inoculated with Plasmodium berghei ANKA strain (PbA) exhibited cerebral symptoms and died from cerebral malaria 6-8 days p.i. whereas DBA/2J mice developed (around days 6-9) a non-fatal cerebral malaria, with milder cerebral symptoms, and died between days 15 and 22 from other malaria-related complications. When inoculated with P. berghei K173 (Pb) these mouse strains did not develop cerebral malaria. These mouse/parasite strain combinations were used, in conjunction with the retinal whole-mount technique, to elucidate factors critical in the pathology of murine cerebral malaria. CBA/T6 mice infected with PbA (PbA-CBA mice) demonstrated mild changes in vascular permeability as early as days 2-3, prior to the appearance on day 5 of cerebral symptoms, whereas mice with non-cerebral malaria did not show any vascular permeability changes until the very late stage of the disease (days 14-22). In the PbA infections, progressive deterioration of endothelial barrier properties, demonstrated by Evans' Blue leakage both generally and from specific focal areas, as well as a developing monocytosis and adherence of mononuclear cells to the endothelium of the retinal vessels continued until death (in CBA/T6 mice) or resolution (in DBA/2J mice). Adherent monocytes, particularly in PbA-CBA mice, were associated with reduced Hoechst staining of individual endothelial cells and a banking up proximally of both parasitized and non-parasitized blood cells in the small blood vessels, often with accompanying focal leakage of Evans' Blue from the retinal vessels. The occurrence and severity of these early changes in the microcirculation correlated with the subsequent development of cerebral symptoms. Monocyte margination appeared to be the most significant factor associated with the development of cerebral symptoms.
接种伯氏疟原虫ANKA株（PbA）的CBA/T6小鼠在感染后6 - 8天出现脑部症状并死于脑型疟疾，而DBA/2J小鼠在感染后6 - 9天左右出现非致命性脑型疟疾，脑部症状较轻，并在15至22天之间死于其他与疟疾相关的并发症。当接种伯氏疟原虫K173（Pb）时，这些小鼠品系未发生脑型疟疾。这些小鼠/寄生虫品系组合与视网膜全层铺片技术相结合，以阐明对鼠脑型疟疾病理学至关重要的因素。感染PbA的CBA/T6小鼠（PbA - CBA小鼠）早在感染后2 - 3天就出现血管通透性轻度变化，早于第5天脑部症状的出现，而患有非脑型疟疾的小鼠直到疾病晚期（14 - 22天）才出现任何血管通透性变化。在PbA感染中，内皮屏障特性逐渐恶化，这通过伊文思蓝在全身和特定局部区域的渗漏得以证明，同时单核细胞增多以及单核细胞黏附于视网膜血管内皮持续到死亡（在CBA/T6小鼠中）或病情缓解（在DBA/2J小鼠中）。黏附的单核细胞，特别是在PbA - CBA小鼠中，与单个内皮细胞的Hoechst染色减少以及小血管中被寄生和未被寄生血细胞在近端的堆积有关，通常伴有视网膜血管伊文思蓝的局部渗漏。这些微循环早期变化的发生和严重程度与随后脑部症状的发展相关。单核细胞靠边似乎是与脑部症状发展相关的最显著因素。
