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鼠疟期间氧化爆发能力的变化及疫苗接种的影响。

Changes in oxidative burst capacity during murine malaria and the effect of vaccination.

作者信息

Dockrell H M, Alavi A, Playfair J H

出版信息

Clin Exp Immunol. 1986 Oct;66(1):37-43.

PMID:3026701
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1542660/
Abstract

Adherent spleen and liver cells from mice infected with Plasmodium yoelii 17X or P. chabaudi AS were tested for production of reactive oxygen intermediates to measure their state of activation. Phorbol myristate acetate (PMA) was used to trigger the respiratory burst and production of superoxide anions was measured by the reduction of nitroblue tetrazolium. Spleen cells from mice infected with P. chabaudi showed an early increase in oxidative activity on day 3, and when the oxidative capacity of the whole spleen was calculated, it was maximal on day 9, just as the mice began to recover. In mice infected with P. yoelii, spleen cells showed an early peak in activity on day 5, and then returned to normal, although the mice did not recover for a further 2-3 weeks. However the total oxidative capacity of the spleen remained high throughout the infection. Mice vaccinated against P. yoelii with a killed blood-stage vaccine showed increased activity on day 3 (spleen) and day 5 (liver), compared with infected control mice. Thus macrophages in these organs could, if given an appropriate trigger, release high levels of these potentially toxic molecules during infection.

摘要

对感染约氏疟原虫17X或查巴迪疟原虫AS的小鼠的贴壁脾细胞和肝细胞进行检测,以测定其活性氧中间体的产生情况,从而衡量它们的激活状态。用佛波酯(PMA)触发呼吸爆发,并通过硝基蓝四唑的还原反应来测定超氧阴离子的产生。感染查巴迪疟原虫的小鼠的脾细胞在第3天氧化活性早期增加,当计算整个脾脏的氧化能力时,在第9天达到最大值,此时小鼠开始恢复。感染约氏疟原虫的小鼠,脾细胞在第5天活性出现早期峰值,然后恢复正常,尽管小鼠在接下来的2 - 3周内并未恢复。然而,在整个感染过程中脾脏的总氧化能力仍然很高。用灭活的血液阶段疫苗接种过约氏疟原虫的小鼠,与感染对照小鼠相比,在第3天(脾脏)和第5天(肝脏)活性增加。因此,这些器官中的巨噬细胞如果受到适当刺激,在感染期间可能会释放大量这些潜在有毒分子。

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本文引用的文献

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Oxidative killing of the intraerythrocytic malaria parasite Plasmodium yoelii by activated macrophages.活化巨噬细胞对红细胞内疟原虫约氏疟原虫的氧化杀伤作用。
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Infect Immun. 1984 Feb;43(2):451-6. doi: 10.1128/iai.43.2.451-456.1984.
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Induction of crisis forms in the human malaria parasite Plasmodium falciparum by gamma-interferon-activated, monocyte-derived macrophages.γ-干扰素激活的单核细胞衍生巨噬细胞诱导人类疟原虫恶性疟原虫形成危机形式。
J Immunol. 1984 Sep;133(3):1601-8.
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