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白细胞介素-1β与肿瘤坏死因子-α协同激活人脐静脉内皮细胞以抑制刚地弓形虫复制。

Co-operation of interleukin-1 beta and tumour necrosis factor-alpha in the activation of human umbilical vein endothelial cells to inhibit Toxoplasma gondii replication.

作者信息

Dimier I H, Bout D T

机构信息

Unité de Recherche Université-INRA d'Immunologie Parasitaire, UFR des Sciences Pharmaceutiques de Tours, Nouzilly, France.

出版信息

Immunology. 1993 Jun;79(2):336-8.

PMID:8344711
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1421863/
Abstract

The tachyzoites of the RH strain of Toxoplasma gondii invaded and replicated in cultured human umbilical vein endothelial cells (HUVEC). Co-treatment of the HUVEC with human recombinant interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) inhibited the replication of T. gondii. Growth of the parasite was measured in vitro by [3H]uracil incorporation assay 18 hr after infection. This assay showed that when cells were pretreated with IL-1 beta and TNF-alpha concentrations ranging from 1 to 100 U/ml, a high degree of inhibition was observed with a phenomenon of co-operation causing a dose-dependent inhibition of the replication of intracellular T. gondii. The mechanism(s) by which the inhibition of multiplication was effected remains to be elucidated.

摘要

刚地弓形虫RH株速殖子侵入培养的人脐静脉内皮细胞(HUVEC)并在其中复制。用人重组白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)共同处理HUVEC可抑制刚地弓形虫的复制。感染18小时后,通过[3H]尿嘧啶掺入试验在体外测定寄生虫的生长。该试验表明,当用浓度范围为1至100 U/ml的IL-1β和TNF-α预处理细胞时,观察到高度抑制,且存在协同作用现象,导致细胞内刚地弓形虫复制受到剂量依赖性抑制。抑制增殖的作用机制尚待阐明。

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Human endothelial cells are activated by IFN-gamma to inhibit Toxoplasma gondii replication. Inhibition is due to a different mechanism from that existing in mouse macrophages and human fibroblasts.人内皮细胞被γ干扰素激活,从而抑制弓形虫的复制。这种抑制作用的机制与小鼠巨噬细胞和人成纤维细胞中存在的机制不同。
J Immunol. 1991 Sep 15;147(6):2019-23.
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A protective role for endogenous tumor necrosis factor in Toxoplasma gondii infection.内源性肿瘤坏死因子在弓形虫感染中的保护作用。
Infect Immun. 1992 May;60(5):1979-83. doi: 10.1128/iai.60.5.1979-1983.1992.