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氯喹在体外可增加恶性疟原虫配子体的形成。

Chloroquine increases Plasmodium falciparum gametocytogenesis in vitro.

作者信息

Buckling A, Ranford-Cartwright L C, Miles A, Read A F

机构信息

Institute of Cell, Animal and Population Biology, Division of Biological Sciences, University of Edinburgh, UK.

出版信息

Parasitology. 1999 Apr;118 ( Pt 4):339-46. doi: 10.1017/s0031182099003960.

Abstract

Malaria parasites are capable of modulating the diversion of resources from asexual growth to the production of stages infective to mosquitoes (gametocytes). Increased rates of gametocytogenesis appear to be a general response to stress, both naturally encountered and novel. We have previously reported earlier and greater gametocytogenesis in response to subcurative antimalarial chemotherapy in the rodent malaria, Plasmodium chabaudi, in vivo. Using an immunofluorescent assay to detect parasites that had invaded red blood cell monolayers, we demonstrate a 5-fold increase in gametocytogenesis in the human malaria, P. falciparum, in vitro, in response to treatment with the antimalarial drug chloroquine. In all clones used, gametocytogenesis increased with increasing inhibition of asexual growth by chloroquine. Furthermore, there were clone differences in the relationship between stress and gametocyte production, implying the response was genetically variable. This was not, however, associated with chloroquine resistance. The epidemiological significance of these results is discussed.

摘要

疟原虫能够调控资源从无性繁殖生长转向产生对蚊子具有感染性的阶段(配子体)。配子体生成率的增加似乎是对自然遇到的应激以及新出现应激的一种普遍反应。我们之前报道过,在啮齿动物疟原虫——查巴迪疟原虫体内,亚治疗剂量的抗疟化疗会导致更早且更多的配子体生成。使用免疫荧光测定法来检测侵入红细胞单层的寄生虫,我们证明,在体外,用抗疟药物氯喹治疗后,人类疟原虫恶性疟原虫的配子体生成增加了5倍。在所有使用的克隆中,配子体生成随着氯喹对无性繁殖生长抑制作用的增强而增加。此外,应激与配子体产生之间的关系存在克隆差异,这意味着该反应具有遗传变异性。然而,这与氯喹抗性无关。文中讨论了这些结果的流行病学意义。

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