Lessons Learned for Pathogenesis, Immunology, and Disease of Erythrocytic Parasites: Plasmodium and Babesia.

Lessons Learned for Pathogenesis, Immunology, and Disease of Erythrocytic Parasites: Plasmodium and Babesia.
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DOI:
10.3389/fcimb.2021.685239
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发表时间:
2021
影响因子:
5.7
通讯作者:
Parveen N
Parveen N
中科院分区:
医学2区
文献类型:
--
作者:
Djokic V;Rocha SC;Parveen N

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由疟原虫属物种引起并由按蚊属蚊子传播的疟疾影响大量人群,而硬蜱属蜱传播巴贝虫属物种并引起巴贝虫病。动物的巴贝斯虫病被认为是一种经济损失,在过去的20-30年里,人类疾病也成为一个严重的医疗保健问题。关于巴氏巴氏杆菌属引起的发病机制、免疫和疾病的文献有限。他们的基因组是最近十年才被测序的因此,我们以以往对疟原虫的研究为基础,比较了巴氏疟原虫的发病机制和宿主免疫反应的异同。这两种血寄生虫在其各自载体中的性生活周期非常相似。一个成年的雌性按蚊一生中可以多次吸血,这样它就可以获得疟原虫并将其传播给宿主。由于每个蜱虫阶段仅取食一次血,因此从幼虫到若虫或若虫到成虫的经幼虫水平传播对于将巴氏蜱释放到宿主中至关重要。这些寄生虫的无性周期的起始是不同的,因为疟原虫子孢子需要在排出的裂殖子可以感染红细胞之前感染肝细胞,而已知巴氏疟原虫子孢子直接进入红细胞周期。疟原虫的代谢,由于其基因组比不同的巴氏疟原虫大两到三倍,因此更为复杂。疟原虫复制发生在宿主细胞内的寄生虫空泡(PV)中,并且在疟原虫生殖后从每个感染的RBC释放相对大量的裂殖子。巴伯氏红细胞周期缺乏PV和卵母细胞生殖。在巴氏疟原虫中,尚没有关于细胞粘附作用的记载,这种细胞粘附作用可使疟原虫(主要是恶性疟原虫)在不同器官中被显著的粘附素所促进。炎性免疫反应导致疟疾和巴贝虫病的严重程度。抗体在这些疾病的解决中似乎只起次要作用;然而,细胞和先天免疫对于清除这两种病原体至关重要。炎症免疫反应影响这两种疾病的严重程度。巨噬细胞促进两种感染的解决,并提供针对相关原生动物的交叉保护。虽然这些寄生虫对适应性免疫反应的免疫抑制似乎不影响它们自身的清除,但它显著加剧了在合并感染期间由合并感染细菌引起的疾病。
Malaria caused by Plasmodium species and transmitted by Anopheles mosquitoes affects large human populations, while Ixodes ticks transmit Babesia species and cause babesiosis. Babesiosis in animals has been known as an economic drain, and human disease has also emerged as a serious healthcare problem in the last 20–30 years. There is limited literature available regarding pathogenesis, immunity, and disease caused by Babesia spp. with their genomes sequenced only in the last decade. Therefore, using previous studies on Plasmodium as the foundation, we have compared similarities and differences in the pathogenesis of Babesia and host immune responses. Sexual life cycles of these two hemoparasites in their respective vectors are quite similar. An adult Anopheles female can take blood meal several times in its life such that it can both acquire and transmit Plasmodia to hosts. Since each tick stage takes blood meal only once, transstadial horizontal transmission from larva to nymph or nymph to adult is essential for the release of Babesia into the host. The initiation of the asexual cycle of these parasites is different because Plasmodium sporozoites need to infect hepatocytes before egressed merozoites can infect erythrocytes, while Babesia sporozoites are known to enter the erythrocytic cycle directly. Plasmodium metabolism, as determined by its two- to threefold larger genome than different Babesia, is more complex. Plasmodium replication occurs in parasitophorous vacuole (PV) within the host cells, and a relatively large number of merozoites are released from each infected RBC after schizogony. The Babesia erythrocytic cycle lacks both PV and schizogony. Cytoadherence that allows the sequestration of Plasmodia, primarily P. falciparum in different organs facilitated by prominent adhesins, has not been documented for Babesia yet. Inflammatory immune responses contribute to the severity of malaria and babesiosis. Antibodies appear to play only a minor role in the resolution of these diseases; however, cellular and innate immunity are critical for the clearance of both pathogens. Inflammatory immune responses affect the severity of both diseases. Macrophages facilitate the resolution of both infections and also offer cross-protection against related protozoa. Although the immunosuppression of adaptive immune responses by these parasites does not seem to affect their own clearance, it significantly exacerbates diseases caused by coinfecting bacteria during coinfections.
DOI: 10.1111/cmi.13350
发表时间: 2021-09
影响因子: 3.4
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Akoolo L;Djokic V;Rocha SC;Parveen N
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