Volf P, Kiewegová A, Svobodová M
Department of Parasitology, Charles University, Prague, Czech Republic.
Med Vet Entomol. 1998 Apr;12(2):151-4. doi: 10.1046/j.1365-2915.1998.00089.x.
Galactosamine, which has been shown in vitro to specifically inhibit sandfly midgut lectin activity, was fed to Phlebotomus duboscqi females with blood containing promastigotes of Leishmania major. Non-inhibitory sugar, galactose, was added in controls. For two strains of L. major (LV 561 and Neal-P), galactosamine substantially enhanced the establishment of infection in the sandfly posterior midgut and significantly increased parasite loads after defaecation, but did not affect anterior migration of Leishmania. On day 3 post-infection, most infections in galactosamine-fed sandfly groups (92% of LV 561 and 100% of Neal-P) were found in the ectoperitrophic space of the posterior midgut, whereas most infections in the galactose-fed groups of sandflies (85% in LV 561 and 96% in Neal-P) were restricted to the peritrophic sac. On day 9, however, the proportion of infections colonizing the stomodeal valve was similar in both dietary groups of sandflies for both strains of L. major. The addition of galactosamine prevented the decrease of parasite loads which occurred in controls between days 3 and 6 post-infection. On days 6 and 9, heavy infections were observed almost exclusively in galactosamine-fed females. Differences between groups were more pronounced for the Neal-P strain, which normally developed poorly in sandflies. Morphology of L. major LV 561 was not affected by galactosamine supplement: the lengths of parasite body and flagellum were similar in both sandfly groups. Two hypotheses are considered for the role of sandfly midgut lectin in Leishmania development in the vector midgut. One proposes that sandfly lectin kills Leishmania promastigotes, the other assumes that lectin blocks LPG-mediated binding of promastigotes to sandfly midgut microvilli.
半乳糖胺在体外已被证明能特异性抑制白蛉中肠凝集素活性，将其与含有硕大利什曼原虫前鞭毛体的血液一起喂给杜氏白蛉雌虫。对照组添加非抑制性糖类半乳糖。对于两株硕大利什曼原虫（LV 561和Neal-P），半乳糖胺显著增强了白蛉后肠感染的建立，并显著增加了排便后寄生虫的负荷，但不影响利什曼原虫的向前迁移。感染后第3天，喂食半乳糖胺的白蛉组中，大多数感染（LV 561组为92%，Neal-P组为l00%）发生在后肠的外营养空间，而喂食半乳糖的白蛉组中，大多数感染（LV 561组为85%，Neal-P组为96%）局限于营养囊。然而，在感染后第9天，对于两株硕大利什曼原虫，两个饮食组的白蛉中定殖于口瓣膜的感染比例相似。添加半乳糖胺可防止对照组在感染后第3天至第6天出现的寄生虫负荷下降。在第6天和第9天，几乎仅在喂食半乳糖胺的雌虫中观察到重度感染。两组之间的差异在Neal-P株中更为明显，该株通常在白蛉中发育较差。半乳糖胺补充剂对硕大利什曼原虫LV 561的形态没有影响：两个白蛉组中寄生虫体和鞭毛的长度相似。关于白蛉中肠凝集素在媒介中肠利什曼原虫发育中的作用，考虑了两种假说。一种假说认为白蛉凝集素杀死利什曼原虫前鞭毛体，另一种假说认为凝集素阻断前鞭毛体通过脂磷壁酸介导与白蛉中肠微绒毛的结合。
