PARASITE SEQUESTRATION IN PLASMODIUM-FALCIPARUM MALARIA - SPLEEN AND ANTIBODY MODULATION OF CYTOADHERENCE OF INFECTED ERYTHROCYTES
PARASITE SEQUESTRATION IN PLASMODIUM-FALCIPARUM MALARIA - SPLEEN AND ANTIBODY MODULATION OF CYTOADHERENCE OF INFECTED ERYTHROCYTES
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DOI：
10.1073/pnas.80.16.5075
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发表时间：
1983-01-01
期刊：
影响因子：
--
通讯作者：
OLIGINO, LD
中科院分区：
文献类型：
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作者：
DAVID, PH;HOMMEL, M;OLIGINO, LD
隔离，即含有晚期发育阶段寄生虫（滋养体和寄生虫）的受感染红细胞粘附于毛细血管和小静脉的内皮，是恶性疟原虫感染的特征。研究了两个宿主因素，脾脏和抗体，影响隔离的恶性疟原虫在松鼠猴。在脾切除动物中，完整动物中发生的滋养体/滋养体感染的红细胞的隔离减少;在体外，当感染的血液与单层人黑素瘤细胞孵育时，来自完整动物的滋养体/滋养体感染的红细胞与黑素瘤细胞结合，但来自脾切除动物的红细胞不与黑素瘤细胞结合。克隆寄生虫感染红细胞的细胞粘附特性从非结合性转变为结合性。免疫血清可以抑制和逆转完整动物感染红细胞与黑色素瘤细胞的体外结合。抗体可以逆转体内隔离，如接种免疫血清后完整动物外周血中出现滋养体/寄生虫感染的红细胞所示。显然，脾脏调节受感染的红细胞膜的寄生虫改变的表达，负责隔离。隔离的预防和逆转可能是抗体介导的抗恶性疟原虫疟疾保护作用的效应机制之一。
Sequestration, the adherence of infected erythrocytes containing late developmental stages of the parasite (trophozoites and schizonts) to the endothelium of capillaries and venules, is characteristic of P. falciparum infections. Two host factors were studied, the spleen and antibody, that influence sequestration of P. falciparum in the squirrel monkey. Sequestration of trophozoite/schizont-infected erythrocytes that occurs in intact animals is reduced in splenectomized animals; in vitro, when infected blood is incubated with monolayers of human melanoma cells, trophozoite/schizont-infected erythrocytes from intact animals, but not from splenectomized animals, bind to the melanoma cells. The switch in cytoadherence characteristics of the infected erythrocytes from nonbinding to binding occurs with a cloned parasite. Immune serum can inhibit and reverse in vitro binding to melanoma cells of infected erythrocytes from intact animals. Antibody can reverse in vivo sequestration, as shown by the appearance of trophozoite/schizont-infected erythrocytes in the peripheral blood of an intact animal after inoculation with immune serum. Apparently, the spleen modulates the expression of parasite alterations of the infected erythrocyte membrane responsible for sequestration. The prevention and reversal of sequestration could be one of the effector mechanisms involved in antibody-mediated protection against P. falciparum malaria.