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首页> 外文期刊>Journal of Parasitology >AGGLUTINATION OF TRYPANOSOMA CRUZI IN INFECTED CELLS TREATED WITH SERUM FROM CHRONICALLY INFECTED MICE
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AGGLUTINATION OF TRYPANOSOMA CRUZI IN INFECTED CELLS TREATED WITH SERUM FROM CHRONICALLY INFECTED MICE

机译：经慢性感染小鼠血清处理的感染细胞中克氏锥虫的凝集作用

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The protozoan parasite Trypanosoma cruzi is the causative agent of Chagas disease. The chronic stage of infection is characterized by a production of neutralizing antibodies in the vertebrate host. A polyclonal antibody, anti-egressin, has been found to inhibit egress of parasites from the host cell late in the intracellular cycle, after the parasites have transformed from the replicative amastigote into the trypomastigote. It has also been found that BALB/c mouse fibroblasts in the late stages of parasite infection become permeable to molecules as large as antibodies, leading to the possibility that anti-egressin affects the intracellular parasites. This project addresses the fate of the intracellular trypomastigotes that have been inhibited from egressing the host cell. Extended cultures of infected fibroblasts treated with chronic mouse serum reduced parasite egress at all time points measured. Parasites released from infected fibroblasts treated with chronic serum had a reduced ability to infect fibroblasts in culture, yet did not lose infectivity entirely. Absorption of chronic serum with living trypomastigotes removed the anti-egressin effect. The possibility that the target of anti-egressin is a parasite surface component is further indicated by the agglutination of extracellular trypomastigotes by chronic serum. The possibility that cross-linking by antibody occurs intracellularly, thus inhibiting egress, was reinforced by cleaving purified IgG into Fab fragments, which did not inhibit egress when added to infected cultures. From this work, it is proposed that the current, best explanation of the mechanism of egress inhibition by anti-egressin is intracellular agglutination, preventing normal parasite-driven egress.
机译：原生动物寄生虫克氏锥虫是南美锥虫病的病原体。感染的慢性阶段的特征是在脊椎动物宿主中产生中和抗体。在寄生虫已从复制性鞭毛虫转变为锥虫病后，已发现一种多克隆抗体抗egressin在细胞内循环后期抑制寄生虫从宿主细胞中逸出。还已经发现，在寄生虫感染的后期，BALB / c小鼠成纤维细胞可渗透至与抗体一样大的分子，从而导致抗出口蛋白影响细胞内寄生虫的可能性。该项目解决了已被抑制逃出宿主细胞的细胞内类拟鞭毛体的命运。在所有测量的时间点，用慢性小鼠血清处理的感染的成纤维细胞的延长培养物降低了寄生虫的流出。从用慢性血清处理过的受感染成纤维细胞释放的寄生虫感染培养物中成纤维细胞的能力降低，但并未完全丧失感染力。用活的类鞭毛鞭毛虫吸收慢性血清可消除抗egressin的作用。抗出口蛋白的靶标是寄生虫表面成分的可能性进一步通过慢性血清对细胞外色鞭毛体的凝集来表明。通过将纯化的IgG裂解为Fab片段，增强了抗体在细胞内发生交联的可能性，从而抑制了流出，当将其加入感染的培养物中时，该片段不会抑制流出。通过这项工作，提出了目前关于抗出口蛋白抑制出口机制的最佳解释是细胞内凝集，防止正常的寄生虫驱动的出口。

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