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脂多糖对红细胞内疟原虫(文氏疟原虫)产生的细胞抑制作用可能源于巨噬细胞。

Probable macrophage origin of the lipopolysaccharide-induced cytostatic effect on intra-erythrocytic malarial parasites (Plasmodium vinckei).

作者信息

Rzepczyk C M

出版信息

Immunology. 1982 Jun;46(2):261-70.

PMID:6282737
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1555380/
Abstract

This study showed that intra-erythrocytic parasites taken from either normal, irradiated, nude or splenectomized mice 7–8 hr after the injection of a small dose of bacterial lipopolysaccharide (LPS) incorporate hypoxanthine more slowly in an assay than parasites from saline-treated controls. The incorporation by parasites of isoleucine, which was also measured in some experiments, was similarly affected. However, this cytostatic effect on parasite metabolism was found to be markedly reduced in experiments with mice which had received an intravenous injection of silica dust 28–30 hr before being injected with LPS. These findings indicate that macrophages, being radioresistant and silica-sensitive, are the source of the cytostatic effect. The present results also imply that T cells are not required in the response, and they show that the host cells mediating this response are not restricted to the spleen. It was also shown that an intravenous injection of a small dose of LPS into mice infected with 24 hr previously, could temporarily arrest the rise in parasitaemia in these animals, thereby prolonging their survival. This protection afforded by LPS was also found to be radioresistant and T-independent. It is suggested that the effect on parasitaemia seen and the cytostatic effect are both due to the release of a soluble factor from macrophages which is ultimately capable of causing intra-erythrocytic parasite death. -infected mice exhibited symptoms of endotoxaemia following the injection of LPS. However, no clear relationship was noted between the severity of the illness in the host and the cytostatic effect on the parasites.

摘要

本研究表明,在注射小剂量细菌脂多糖(LPS)7 - 8小时后,从正常、经辐照、裸鼠或脾切除小鼠体内获取的红细胞内寄生虫,在检测中次黄嘌呤的掺入速度比生理盐水处理的对照组寄生虫更慢。在一些实验中也检测的异亮氨酸掺入情况,寄生虫的掺入也受到类似影响。然而,在给小鼠静脉注射二氧化硅粉尘28 - 30小时后再注射LPS的实验中,发现这种对寄生虫代谢的细胞抑制作用明显降低。这些发现表明,巨噬细胞具有抗辐射性且对二氧化硅敏感,是细胞抑制作用的来源。目前的结果还表明,该反应不需要T细胞,并且表明介导这种反应的宿主细胞不限于脾脏。还表明,对24小时前感染的小鼠静脉注射小剂量LPS,可暂时阻止这些动物体内寄生虫血症的上升,从而延长它们的存活时间。LPS提供的这种保护作用也被发现具有抗辐射性且不依赖T细胞。有人提出,观察到的对寄生虫血症的影响和细胞抑制作用均归因于巨噬细胞释放的一种可溶性因子,该因子最终能够导致红细胞内寄生虫死亡。感染的小鼠在注射LPS后出现内毒素血症症状。然而,未观察到宿主疾病严重程度与对寄生虫的细胞抑制作用之间存在明确关系。

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Immunology. 1982 Jun;46(2):261-70.
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引用本文的文献

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本文引用的文献

1
The role of the liver in immunity to blood-stage murine malaria.肝脏在小鼠血液期疟疾免疫中的作用。
Immunology. 1980 Oct;41(2):421-30.
2
Demonstration of a lipopolysaccharide-induced cytostatic effect on malarial parasites.脂多糖对疟原虫的细胞生长抑制作用的证明。
Infect Immun. 1981 Aug;33(2):343-7. doi: 10.1128/iai.33.2.343-347.1981.
3
Endotoxin-induced serum factor kills malarial parasites in vitro.内毒素诱导的血清因子在体外可杀死疟原虫。
Infect Immun. 1981 Jul;33(1):83-9. doi: 10.1128/iai.33.1.83-89.1981.
4
Two distinct types of non-specific immunosuppression in murine malaria.小鼠疟疾中两种不同类型的非特异性免疫抑制。
Clin Exp Immunol. 1980 Dec;42(3):428-35.
5
Resolution of acute malaria (Plasmodium berghei in the rat): reversibility and spleen dependence.急性疟疾(大鼠体内的伯氏疟原虫)的消退:可逆性及对脾脏的依赖性
Am J Trop Med Hyg. 1980 Jan;29(1):1-4. doi: 10.4269/ajtmh.1980.29.1.
6
Immunity to Plasmodium chabaudi adami in the B-cell-deficient mouse.B细胞缺陷小鼠对查巴迪疟原虫的免疫
Nature. 1981 Mar 12;290(5802):143-5. doi: 10.1038/290143a0.
7
Possible importance of macrophage-derived mediators in acute malaria.巨噬细胞衍生介质在急性疟疾中的潜在重要性。
Infect Immun. 1981 Jun;32(3):1058-66. doi: 10.1128/iai.32.3.1058-1066.1981.
8
Effect of bacterial endotoxin on the course of Plasmodium berghei infection.细菌内毒素对伯氏疟原虫感染病程的影响。
Exp Parasitol. 1967 Apr;20(2):186-99. doi: 10.1016/0014-4894(67)90038-0.
9
Endotoxin-induced modification of Plasmodium berghei infection in mice.内毒素诱导的小鼠伯氏疟原虫感染的改变
J Immunol. 1969 Jan;102(1):131-9.
10
Babesia microti and Plasmodium berghei yoelii infections in nude mice.微小巴贝斯虫和约氏疟原虫在裸鼠中的感染
Nature. 1974 Nov 22;252(5481):328-9. doi: 10.1038/252328a0.