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本文引用的文献

1
Molecular evidence for the localization of Plasmodium falciparum immature gametocytes in bone marrow.疟原虫不成熟配子体在骨髓中定位的分子证据。
Blood. 2014 Feb 13;123(7):959-66. doi: 10.1182/blood-2013-08-520767. Epub 2013 Dec 13.
2
Enhanced gametocyte formation in erythrocyte progenitor cells: a site-specific adaptation by Plasmodium falciparum.增强红系祖细胞中的配子体形成:恶性疟原虫的一个特异性适应。
J Infect Dis. 2013 Oct 1;208(7):1170-4. doi: 10.1093/infdis/jit309. Epub 2013 Jul 11.
3
Early gametocytes of the malaria parasite Plasmodium falciparum specifically remodel the adhesive properties of infected erythrocyte surface.恶性疟原虫的早期配子体特异性重塑被感染红细胞表面的黏附特性。
Cell Microbiol. 2013 Apr;15(4):647-59. doi: 10.1111/cmi.12062. Epub 2012 Nov 21.
4
The extravascular compartment of the bone marrow: a niche for Plasmodium falciparum gametocyte maturation?骨髓的血管外腔隙:恶性疟原虫配子体成熟的小生境?
Malar J. 2012 Aug 20;11:285. doi: 10.1186/1475-2875-11-285.
5
A switch in infected erythrocyte deformability at the maturation and blood circulation of Plasmodium falciparum transmission stages.疟原虫传播阶段成熟和血液循环中受感染红细胞变形能力的转变。
Blood. 2012 Jun 14;119(24):e172-80. doi: 10.1182/blood-2012-03-414557. Epub 2012 Apr 18.
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Host cell deformability is linked to transmission in the human malaria parasite Plasmodium falciparum.宿主细胞的变形能力与人类疟原虫 Plasmodium falciparum 的传播有关。
Cell Microbiol. 2012 Jul;14(7):983-93. doi: 10.1111/j.1462-5822.2012.01786.x. Epub 2012 Apr 12.
7
Differential adhesive properties of sequestered asexual and sexual stages of Plasmodium falciparum on human endothelial cells are tissue independent.疟原虫无性体和有性体在人内皮细胞上的差异黏附特性与组织无关。
PLoS One. 2012;7(2):e31567. doi: 10.1371/journal.pone.0031567. Epub 2012 Feb 21.
8
Proof of principle for transfusion of in vitro-generated red blood cells.体外生成红细胞输注的原理验证。
Blood. 2011 Nov 10;118(19):5071-9. doi: 10.1182/blood-2011-06-362038. Epub 2011 Sep 1.
9
Consequences of HIV infection on malaria and therapeutic implications: a systematic review.HIV 感染对疟疾的影响及治疗意义:系统评价。
Lancet Infect Dis. 2011 Jul;11(7):541-56. doi: 10.1016/S1473-3099(11)70031-7.
10
Protein targeting to the parasitophorous vacuole membrane of Plasmodium falciparum.蛋白质靶向恶性疟原虫的寄生泡膜
Eukaryot Cell. 2011 Jun;10(6):744-52. doi: 10.1128/EC.00008-11. Epub 2011 Apr 15.

恶性疟原虫传播阶段在人类骨髓中聚集。

Plasmodium falciparum transmission stages accumulate in the human bone marrow.

作者信息

Joice Regina, Nilsson Sandra K, Montgomery Jacqui, Dankwa Selasi, Egan Elizabeth, Morahan Belinda, Seydel Karl B, Bertuccini Lucia, Alano Pietro, Williamson Kim C, Duraisingh Manoj T, Taylor Terrie E, Milner Danny A, Marti Matthias

机构信息

Department of Immunology and Infectious Diseases, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA.

Malawi-Liverpool-Wellcome Trust Clinical Research Programme, P. O. Box 30096, Chichiri, Blantyre 3, Malawi. Liverpool School of Tropical Medicine, University of Liverpool, Liverpool L3 5QA, UK.

出版信息

Sci Transl Med. 2014 Jul 9;6(244):244re5. doi: 10.1126/scitranslmed.3008882.

DOI:10.1126/scitranslmed.3008882
PMID:25009232
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4175394/
Abstract

Transmission of Plasmodium falciparum malaria parasites requires formation and development of gametocytes, yet all but the most mature of these sexual parasite forms are absent from the blood circulation. We performed a systematic organ survey in pediatric cases of fatal malaria to characterize the spatial dynamics of gametocyte development in the human host. Histological studies revealed a niche in the extravascular space of the human bone marrow where gametocytes formed in erythroid precursor cells and underwent development before reentering the circulation. Accumulation of gametocytes in the hematopoietic system of human bone marrow did not rely on cytoadherence to the vasculature as does sequestration of asexual-stage parasites. This suggests a different mechanism for the sequestration of gametocytes that could potentially be exploited to block malaria transmission.

摘要

恶性疟原虫疟原虫的传播需要配子体的形成和发育,然而,除了最成熟的这些有性寄生虫形式外,血液循环中几乎不存在其他形式。我们对致命疟疾的儿科病例进行了系统的器官调查,以描述人类宿主中配子体发育的空间动态。组织学研究揭示了人类骨髓血管外空间中的一个生态位,配子体在红细胞前体细胞中形成,并在重新进入循环之前在此处发育。人类骨髓造血系统中配子体的积累并不像无性阶段寄生虫的滞留那样依赖于对脉管系统的细胞粘附。这表明存在一种不同的配子体滞留机制,有可能被利用来阻断疟疾传播。