Species-specific escape of Plasmodium sporozoites from oocysts of avian, rodent, and human malarial parasites.
Species-specific escape of Plasmodium sporozoites from oocysts of avian, rodent, and human malarial parasites.
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DOI：
10.1186/s12936-016-1451-y
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发表时间：
2016-08-02
期刊：
影响因子：
3
通讯作者：
Pimenta PF
中科院分区：
文献类型：
--
作者：
Orfano AS;Nacif-Pimenta R;Duarte AP;Villegas LM;Rodrigues NB;Pinto LC;Campos KM;Pinilla YT;Chaves B;Barbosa Guerra MG;Monteiro WM;Smith RC;Molina-Cruz A;Lacerda MV;Secundino NF;Jacobs-Lorena M;Barillas-Mury C;Pimenta PF
当受感染的蚊子将疟原虫子孢子传播到脊椎动物宿主体内时，疟疾就会传播。疟原虫有很多种，一般来说，感染是宿主特异性的。例如，鸡疟原虫是一种禽类寄生虫，而伯氏疟原虫则感染小鼠。这两种寄生虫已被广泛用作疟疾传播的实验模型。恶性疟原虫和间日疟原虫是人类疟疾最重要的病原体，疟疾是一种全球性的危及生命的疾病。为了完成其生命周期，疟原虫寄生虫必须穿过蚊子中肠并形成不断分裂的卵囊。成熟的卵囊将数千个子孢子释放到蚊子的血淋巴中，这些子孢子必须到达唾液腺才能感染新的脊椎动物宿主。目前对卵囊形成和子孢子释放生物学的理解主要基于伯氏疟原虫的实验感染，并且将结论推广到感染人类的其他疟原虫物种，而无需进一步的形态学分析。在这里，描述了从四种疟原虫卵囊中逸出子孢子的显微解剖结构：两种实验室模型鸡疟原虫和伯氏疟原虫，以及引起人类疟疾的两种主要物种间日疟原虫和恶性疟原虫。研究发现子孢子具有物种特异性的卵囊逃逸机制。疟原虫的两种模式物种具有共同的机制，即卵囊壁在子孢子出现之前破裂。相比之下，间日疟原虫和恶性疟原虫子孢子表现出通过极化推进从卵囊中动态逃逸的机制。这项研究表明，疟原虫物种并不像之前认为的那样具有共同的子孢子逃逸机制，而是表现出复杂且物种特异性的机制。此外，了解人类疟原虫中的这种现象可以促进传播阻断研究，而不仅仅是基于鼠类和鸟类模型的研究。
Malaria is transmitted when an infected mosquito delivers Plasmodium sporozoites into a vertebrate host. There are many species of Plasmodium and, in general, the infection is host-specific. For example, Plasmodium gallinaceum is an avian parasite, while Plasmodium berghei infects mice. These two parasites have been extensively used as experimental models of malaria transmission. Plasmodium falciparum and Plasmodium vivax are the most important agents of human malaria, a life-threatening disease of global importance. To complete their life cycle, Plasmodium parasites must traverse the mosquito midgut and form an oocyst that will divide continuously. Mature oocysts release thousands of sporozoites into the mosquito haemolymph that must reach the salivary gland to infect a new vertebrate host. The current understanding of the biology of oocyst formation and sporozoite release is mostly based on experimental infections with P.berghei, and the conclusions are generalized to other Plasmodium species that infect humans without further morphological analyses. Here, it is described the microanatomy of sporozoite escape from oocysts of four Plasmodium species: the two laboratory models, P. gallinaceum and P. berghei, and the two main species that cause malaria in humans, P.vivax and P. falciparum. It was found that sporozoites have species-specific mechanisms of escape from the oocyst. The two model species of Plasmodium had a common mechanism, in which the oocyst wall breaks down before sporozoites emerge. In contrast, P. vivax and P. falciparum sporozoites show a dynamic escape mechanism from the oocyst via polarized propulsion. This study demonstrated that Plasmodium species do not share a common mechanism of sporozoite escape, as previously thought, but show complex and species-specific mechanisms. In addition, the knowledge of this phenomenon in human Plasmodium can facilitate transmission-blocking studies and not those ones only based on the murine and avian models.