Dhume S T, Adams-Burton C R, Shumak K H, Laine R A
Department of Biochemistry, Louisiana State University, Baton Rouge 70803, USA.
Glycobiology. 1994 Dec;4(6):903-8. doi: 10.1093/glycob/4.6.903.
A HEMPAS (hereditary erythroblastic multinuclearity with positive acidified serum test) erythrocyte, atypical Variant II (referred to herein as Variant II-gal-), lacking long-chain polylactosamine on both glycoproteins (Band 3 and 4.5) and glycosphingolipids, was characterized by the carbohydrate profile of the erythrocyte membrane according to Fukuda et al. (Blood, 73, 1331-1339, 1989). Two laboratories previously reported that polylactosamine isolated from the erythrocyte protein Band 3 inhibited invasion of red blood cells by Plasmodium falciparum in malarial culture, suggesting a role for this carbohydrate in adhesion of the parasite. Therefore, HEMPAS erythrocyte Variant II-gal- presented a unique opportunity to further examine this premise. Freshly drawn blood samples (normal and HEMPAS Variant II-gal-) were separately incubated with P. falciparum from mannitol-synchronized cultures. The parasite was found to invade HEMPAS Variant II-gal- erythrocytes at a 30% lower rate through two life cycles, as shown by microscopic evaluation of invasion and by [3H]hypoxanthine incorporation into parasite. This observation, along with the published fact that glycophorin-deficient MkMk cells are also infectable, but at a lower rate, indicates that neither sialoglycoproteins nor polylactosamines are an obligate adhesive ligand for P. falciparum, although the possibility remains that either may still contribute to adhesive events during infection.
根据福田等人（《血液》，第73卷，第1331 - 1339页，1989年）的研究，一种遗传性红细胞多核性伴酸化血清试验阳性（HEMPAS）的红细胞，即非典型变体II（本文中称为变体II - gal -），其糖蛋白（带3和带4.5）和糖鞘脂上均缺乏长链聚乳糖胺，通过红细胞膜的碳水化合物谱得以表征。此前有两个实验室报告称，从红细胞蛋白带3中分离出的聚乳糖胺可抑制恶性疟原虫在疟疾培养物中对红细胞的入侵，这表明这种碳水化合物在寄生虫黏附中发挥作用。因此，HEMPAS红细胞变体II - gal -为进一步检验这一前提提供了独特的机会。将新鲜采集的血液样本（正常样本和HEMPAS变体II - gal -样本）分别与来自甘露醇同步培养物的恶性疟原虫一起孵育。通过对入侵的显微镜评估以及[3H]次黄嘌呤掺入寄生虫的情况表明，在两个生命周期中，该寄生虫入侵HEMPAS变体II - gal -红细胞的速率要低30%。这一观察结果，连同已发表的事实，即缺乏血型糖蛋白的MkMk细胞也可被感染，但感染率较低，表明唾液酸糖蛋白和聚乳糖胺都不是恶性疟原虫必不可少的黏附配体，尽管仍有可能它们在感染过程中仍对黏附事件有一定作用。
