Plasmodium chabaudi-infected erythrocytes adhere to CD36 and bind to microvascular endothelial cells in an organ-specific way
Plasmodium chabaudi-infected erythrocytes adhere to CD36 and bind to microvascular endothelial cells in an organ-specific way
复制标题
DOI：
10.1128/iai.68.7.4135-4144.2000
复制
发表时间：
2000-07-01
影响因子：
3.1
通讯作者：
Holder, AA
中科院分区：
文献类型：
--
作者：
Mota, MM;Jarra, W;Holder, AA
恶性疟原虫感染红细胞粘附于微血管内皮细胞（隔离）被认为在疟原虫毒力和发病机制中起重要作用，然而隔离对感染和疾病的真实的重要性从未被充分评估。缺乏一个合适的体内模型隔离一直是一个主要的障碍，我们已经检查了啮齿动物疟原虫夏氏疟原虫在小鼠作为一个潜在的模型。感染这种寄生虫的红细胞在体外粘附于纯化的CD 36，CD 36是结合恶性疟原虫感染的红细胞的关键内皮受体。P. C.在体外，感染夏保迪的红细胞以γ-干扰素依赖性方式粘附于内皮细胞，这表明在结合过程中涉及另外的粘附分子，恶性疟原虫感染的细胞也是如此。此外，分别来自感染和超免疫小鼠的血浆或血清具有阻断感染的红细胞与内皮细胞结合的能力。在体内，含有成熟P. c.查鲍迪寄生虫从外周循环中隔离出来。隔离是器官特异性的，主要发生在肝脏中，尽管在脾脏和大脑中也观察到感染的红细胞和内皮细胞之间的密切接触。结果进行了讨论的背景下，使用该模型来研究（i）内皮细胞活化和隔离水平之间的关系和（ii）隔离在疟疾感染的主要功能。
Adherence of erythrocytes infected with Plasmodium falciparum to microvascular endothelial cells (sequestration) is considered to play an important role in parasite virulence and pathogenesis, However, the real importance of sequestration for infection and disease has never been fully assessed. The absence of an appropriate in vivo model far sequestration has been a major barrier, We have examined the rodent malaria parasite Plasmodium chabaudi chabaudi AS in mice as a potential model. Erythrocytes infected with this parasite adhere in vitro to purified CD36, a critical endothelium receptor for binding P. falciparum-infected erythrocytes. P. c. chabaudi-infected erythrocytes adhere in vitro to endothelial cells in a gamma interferon-dependent manner, suggesting the involvement of additional adhesion molecules in the binding process, as is also the case with P. falciparum-infected cells. Furthermore, plasma or sera from infected and hyperimmune mice, respectively, have the ability to block binding of infected erythrocytes to endothelial cells. In vivo, erythrocytes containing mature P. c. chabaudi parasites are sequestered from the peripheral circulation. Sequestration is organ specific, occurring primarily in the liver, although intimate contact between infected erythrocytes and endothelial cells is also observed in the spleen and brain. The results are discussed in the context of the use of this model to study (i) the relationship between endothelial cell activation and the level of sequestration and (ii) the primary function of sequestration in malaria infection.