Zehavi U, El-On J, Pearlman E, Abrahams J C, Greenblatt C L
Z Parasitenkd. 1983;69(4):405-14. doi: 10.1007/BF00927696.
Leishmania tropica promastigotes are easily attached to and engulfed by C3H peritoneal macrophages in vitro at 37 degrees C. Different sugars at 0.3-0.5 M inhibited in vitro the attachment of L. tropica promastigotes to C3H peritoneal macrophages with lactose (Gal-beta [1 leads to 4]Glc) being the most efficient. Inhibition of attachment is also affected by pre-treatment of promastigotes with galactose oxidase. Oligosaccharides extending from promastigote and amastigote cell surfaces contain an important proportion of non-reducing galactose as does the carbohydrate-rich factor (EF) excreted by promastigotes of L. tropica and L. donovani. This study suggests that Leishmania, an obligatory intracellular parasite, uses as a means of entering the host cell a cellular mechanism similar to that used in the removal of damaged cells from blood circulation. This mechanism is assumed to take advantage of the exposed sugars, particularly the exposed non-reducing galactose, on the parasite surface during the stage of attachment. Once the parasite is inside the cell, the EF it produces might have a protective function, being inhibitory to some of the host cell lysosomal enzymes.
热带利什曼原虫前鞭毛体在37℃体外培养时很容易被C3H腹膜巨噬细胞附着并吞噬。0.3 - 0.5M的不同糖类在体外可抑制热带利什曼原虫前鞭毛体与C3H腹膜巨噬细胞的附着,其中乳糖(半乳糖-β[1→4]葡萄糖)最为有效。用半乳糖氧化酶预处理前鞭毛体也会影响附着的抑制作用。从利什曼原虫前鞭毛体和无鞭毛体细胞表面延伸出的寡糖含有重要比例的非还原半乳糖,热带利什曼原虫和杜氏利什曼原虫前鞭毛体分泌的富含碳水化合物的因子(EF)也是如此。本研究表明,利什曼原虫作为一种专性细胞内寄生虫,利用一种类似于从血液循环中清除受损细胞的细胞机制进入宿主细胞。该机制被认为是在附着阶段利用了寄生虫表面暴露的糖类,特别是暴露的非还原半乳糖。一旦寄生虫进入细胞内,它产生的EF可能具有保护作用,对宿主细胞的一些溶酶体酶具有抑制作用。