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用弓形虫攻击后J774G8细胞和小鼠腹腔巨噬细胞的淋巴因子激活

Lymphokine activation of J774G8 cells and mouse peritoneal macrophages challenged with Toxoplasma gondii.

作者信息

Sibley L D, Krahenbuhl J L, Weidner E

出版信息

Infect Immun. 1985 Sep;49(3):760-4. doi: 10.1128/iai.49.3.760-764.1985.

Abstract

In vitro activation of macrophage cell line J774G8 and mouse peritoneal macrophages resulted in oxygen-dependent and oxygen-independent killing of intracellular Toxoplasma gondii. Activation was characterized by oxygen-dependent killing detectable by enhanced lysosome fusion and digestion of T. gondii. The toxoplasmacidal activity of activated J774G8 cells and peritoneal macrophages was prevented by adding the oxygen intermediate scavengers catalase or superoxide dismutase during culture. Activated J774G8 cells and peritoneal macrophages also inhibited replication of those Toxoplasma organisms which survived the initial microbicidal activity. The inhibition of Toxoplasma replication was not significantly affected by exogenous catalase or superoxide dismutase. Peritoneal macrophages from Toxoplasma-immune mice showed similar microbicidal and inhibitory responses, supporting the model that activation leads to destruction of intracellular parasites by two different mechanisms.

摘要

巨噬细胞系J774G8和小鼠腹腔巨噬细胞的体外激活导致对细胞内刚地弓形虫的需氧和非需氧杀伤。激活的特征是通过增强溶酶体融合和对刚地弓形虫的消化来检测到需氧杀伤。在培养过程中添加氧中间体清除剂过氧化氢酶或超氧化物歧化酶可阻止激活的J774G8细胞和腹腔巨噬细胞的杀弓形虫活性。激活的J774G8细胞和腹腔巨噬细胞也抑制了那些在初始杀菌活性中存活下来的弓形虫生物体的复制。过氧化氢酶或超氧化物歧化酶对外源弓形虫复制的抑制作用没有显著影响。来自弓形虫免疫小鼠的腹腔巨噬细胞表现出类似的杀菌和抑制反应,支持了激活通过两种不同机制导致细胞内寄生虫破坏的模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/648e/261267/8c1167e42163/iai00114-0309-a.jpg

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