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恶性疟原虫感染胎盘组织中硫酸软骨素A表达的定量计算机图像分析

Quantitative computer image analysis of chondroitin sulfate A expression in placentas infected with Plasmodium falciparum.

作者信息

Sartelet H, Garraud O, Lorenzato M, Rogier C, Milko-Sartelet I, Huerre M, Gaillard D

机构信息

Departments of Pathology and Pediatrics, Hôpital Principal, Dakar, Senegal.

出版信息

J Histochem Cytochem. 1999 Jun;47(6):751-6. doi: 10.1177/002215549904700604.

Abstract

Most pathological conditions resulting from infection with the human malaria parasite Plasmodium falciparum occur as a consequence of the sequestration by several adhesion molecules of parasite-infected red blood cells (IRBCs). Recent reports have provided evidence that placental vascular endothelial ligands for IRBCs were mostly restricted to chondroitin sulfate A (CSA). The expression of CSA in malaria-infected placentas was investigated in a prospective case-control study in a hypoendemic area (Dakar, Senegal). The tissue distribution of CSA was measured in the terminal villi by immunostaining combined with image processing in 20 infected and 20 noninfected frozen sections of placenta. The villous surface immunostained by anti-CSA antibody was higher in infected than in noninfected placentas (p<0.03), in placentas with active infection than in those with past chronic infection (p<0.05), and in infected placentas with positive imprints than in those with negative imprints (not significant; p=0.06). Labeling was found in the extracellular matrix and in endothelial and stromal cells of all the placentas. Syncytiotrophoblast immunostaining was detected in all placentas associated with active or active chronic infection (n=7) but in only 4/13 placentas with past chronic infection (p<0.01). The presence of P. falciparum in the imprint was significantly correlated with immunostaining of CSA in syncytiotrophoblasts (p=0.003). These results suggest that CSA can play an important role in the sequestration of P. falciparum in human placentas during the acute phase of infection.

摘要

由人类疟原虫恶性疟原虫感染导致的大多数病理状况,是由几种粘附分子介导的寄生虫感染红细胞(IRBCs)滞留所致。最近的报告提供了证据,表明IRBCs的胎盘血管内皮配体大多局限于硫酸软骨素A(CSA)。在一个低流行地区(塞内加尔达喀尔)进行的一项前瞻性病例对照研究中,对疟疾感染胎盘内CSA的表达进行了调查。通过免疫染色结合图像处理技术,在20份感染胎盘和20份未感染胎盘的冰冻切片的终末绒毛中测量CSA的组织分布。抗CSA抗体免疫染色的绒毛表面,在感染胎盘比未感染胎盘更高(p<0.03),在有活动性感染的胎盘比既往慢性感染的胎盘更高(p<0.05),在有阳性印记的感染胎盘比有阴性印记的感染胎盘更高(无显著性差异;p=0.06)。在所有胎盘的细胞外基质以及内皮细胞和基质细胞中均发现有标记。在所有与活动性或活动性慢性感染相关的胎盘(n=7)中均检测到合体滋养层免疫染色,但在仅4/13份既往慢性感染的胎盘中检测到(p<0.01)。印记中恶性疟原虫的存在与合体滋养层中CSA的免疫染色显著相关(p=0.003)。这些结果表明,CSA在感染急性期人类胎盘中恶性疟原虫的滞留过程中可能起重要作用。

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