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首页> 外文期刊>Infection and immunity >Role of immune serum and complement in stimulation of the metabolic burst of human neutrophils by Plasmodium falciparum.
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Role of immune serum and complement in stimulation of the metabolic burst of human neutrophils by Plasmodium falciparum.

机译：免疫血清和补体在恶性疟原虫刺激人中性粒细胞代谢爆发中的作用。

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摘要

Interaction between human neutrophils (polymorphonuclear leukocytes [PMN]) and Plasmodium falciparum in the natural defense of the host remains to be elucidated. In patients with acute malaria, oxygen consumption (QO2) of PMN at rest and after stimulation by zymosan was significantly increased compared with that in the controls. With 10% immune serum, both QO2 and chemiluminescence of normal PMN were significantly increased after stimulation by a P. falciparum erythrocyte culture. This activation was not observed with a nonparasitized erythrocyte culture and was correlated with parasitemia. Immune serum and complement were required to trigger this metabolic activation of normal PMN. With normal serum or heat-inactivated immune serum, a parasitized erythrocyte culture did not significantly stimulate QO2 or chemiluminescence of normal PMN. The classical complement pathway was essential for this stimulation, whereas the alternate pathway was less involved. Hyperimmune sera from subjects residing in endemic areas were more able to trigger the metabolic burst than were immune sera from subjects from other sources. The use of synchronous cultures showed that PMN were more stimulated by cultures rich in merozoites than by the same cultures which contained only intraerythrocytic forms. Giemsa staining showed granules of hemozoin and occasional merozoites or parasitized erythrocytes within PMN. This increase in production of activated oxygen radicals could damage intra-or extraphagocytic parasitic forms. As P. falciparum is sensitive to oxidant stress and PMN is the phagocyte with the most intense metabolic burst, the role of PMN in defense against malaria should be considered.
机译：人类嗜中性粒细胞（多形核白细胞[PMN]）与恶性疟原虫在宿主自然防御中的相互作用尚待阐明。与对照组相比，在急性疟疾患者中，静止和经酵母聚糖刺激后PMN的耗氧量（QO2）显着增加。恶性疟原虫红细胞培养物刺激后，使用10％的免疫血清，正常PMN的QO2和化学发光均显着增加。在未寄生化的红细胞培养物中未观察到这种激活，并且与寄生虫血症相关。需要免疫血清和补体来触发正常PMN的这种代谢活化。使用正常血清或热灭活的免疫血清，被寄生的红细胞培养物不会显着刺激正常PMN的QO2或化学发光。经典补体途径对于这种刺激是必不可少的，而替代途径则较少参与。居住在流行地区的受试者的超免疫血清比其他来源的受试者的免疫血清更有能力触发新陈代谢。同步培养的使用表明，富含裂殖子的培养比仅含红细胞内形式的相同培养对PMN的刺激更大。 Giemsa染色显示PMN内有血红蛋白颗粒，偶有裂殖子或被寄生的红细胞。活性氧自由基产生的增加可能会破坏吞噬细胞内或吞噬细胞外的寄生形式。由于恶性疟原虫对氧化应激敏感，PMN是代谢爆发最剧烈的吞噬细胞，因此应考虑PMN在防御疟疾中的作用。

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