Plasmodium vivax Adherence to Placental Glycosaminoglycans
Plasmodium vivax Adherence to Placental Glycosaminoglycans
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DOI：
10.1371/journal.pone.0034509
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发表时间：
2012-04-17
期刊：
影响因子：
3.7
通讯作者：
White, Nicholas J.
中科院分区：
文献类型：
--
作者：
Chotivanich, Kesinee;Udomsangpetch, Rachanee;White, Nicholas J.
背景：间日疟原虫感染很少直接致死，但确实会通过降低出生体重和引起流产而引起间接死亡。细胞粘附和隔离在微血管中的严重恶性疟原虫疟疾的发病机制是中央的，但在其他人类malarias.Methodology的病理细胞粘附的贡献是不太清楚：粘附性质的间日疟原虫感染的红细胞（PvIRBC）进行了评价，在静态和流动conditions.Principal调查结果：间日疟原虫分离33例进行了研究。没有粘附到固定的CD 36，ICAM-1，或血小板反应蛋白，恶性疟原虫血管细胞粘附的假定配体，或脐静脉内皮细胞，但所有粘附到固定的硫酸软骨素A（CSA）和透明质酸（HA），胎盘中恶性疟原虫粘附的受体。PvIRBC也粘附于新鲜胎盘细胞（N = 5）。用软骨素酶预孵育防止PvIRBC粘附于CSA，并减少与HA的结合，而用透明质酸酶预孵育防止粘附于HA，但不显著减少与CSA的结合。PvIRBC与可溶性CSA和HA的预孵育减少了与固定化受体的结合并防止了胎盘结合。通过与胰蛋白酶预孵育防止PvIRBC粘附，通过肝素抑制PvIRBC粘附，并且通过EGTA减少PvIRBC粘附。在层流条件下，平均（SD）剪切应力使最大附着力降低50%，为0.06（0.02）Pa，但在粘附后，PvIRBC可抵抗高达5 Pa的应力引起的分离。在37 ℃下，粘附在红细胞侵入后约16小时开始，在30小时时粘附最大。在39 ℃时粘附开始较早，并在24小时达到高峰。意义：间日疟原虫感染的红细胞粘附糖胺聚糖可能有助于间日疟的发病机制，并导致宫内发育迟缓。
Background: Plasmodium vivax infections seldom kill directly but do cause indirect mortality by reducing birth weight and causing abortion. Cytoadherence and sequestration in the microvasculature are central to the pathogenesis of severe Plasmodium falciparum malaria, but the contribution of cytoadherence to pathology in other human malarias is less clear.Methodology: The adherence properties of P. vivax infected red blood cells (PvIRBC) were evaluated under static and flow conditions.Principal Findings: P. vivax isolates from 33 patients were studied. None adhered to immobilized CD36, ICAM-1, or thrombospondin, putative ligands for P. falciparum vascular cytoadherence, or umbilical vein endothelial cells, but all adhered to immobilized chondroitin sulphate A (CSA) and hyaluronic acid (HA), the receptors for adhesion of P. falciparum in the placenta. PvIRBC also adhered to fresh placental cells (N = 5). Pre-incubation with chondroitinase prevented PvIRBC adherence to CSA, and reduced binding to HA, whereas preincubation with hyaluronidase prevented adherence to HA, but did not reduce binding to CSA significantly. Pre-incubation of PvIRBC with soluble CSA and HA reduced binding to the immobilized receptors and prevented placental binding. PvIRBC adhesion was prevented by pre-incubation with trypsin, inhibited by heparin, and reduced by EGTA. Under laminar flow conditions the mean (SD) shear stress reducing maximum attachment by 50% was 0.06 (0.02) Pa but, having adhered, the PvIRBC could then resist detachment by stresses up to 5 Pa. At 37 degrees C adherence began approximately 16 hours after red cell invasion with maximal adherence at 30 hours. At 39 degrees C adherence began earlier and peaked at 24 hours.Significance: Adherence of P. vivax-infected erythrocytes to glycosaminoglycans may contribute to the pathogenesis of vivax malaria and lead to intrauterine growth retardation.