活化的小胶质细胞通过一氧化氮机制抑制弓形虫的增殖。

Activated microglia inhibit multiplication of Toxoplasma gondii via a nitric oxide mechanism.

作者信息

Chao C C, Anderson W R, Hu S, Gekker G, Martella A, Peterson P K

机构信息

Neuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, Minnesota 55404.

出版信息

Clin Immunol Immunopathol. 1993 May;67(2):178-83. doi: 10.1006/clin.1993.1062.

DOI:10.1006/clin.1993.1062

PMID:8519093

Abstract

The role of microglia in host defense against Toxoplasma gondii is unknown. In the present study, we investigated the multiplication of T. gondii tachyzoites in murine microglial cell cultures. T. gondii multiplied readily in these cells; multiplication was prevented when microglia were activated with interferon-gamma plus lipopolysaccharide, a treatment that also upregulates nitric oxide (NO) synthase activity. Simultaneous treatment of microglial cell cultures with activation signals and the NO synthase inhibitor NG-monomethyl-L-arginine (NGMA) prevented the antitoxoplasmic activity. Transmission electron microscopic analysis demonstrated degenerative tachyzoites in activated microglia but not in control or NGMA groups. These findings support the view that the host defense function of activated microglia against T. gondii involves generation of the free radical NO.

摘要

小胶质细胞在宿主抵御刚地弓形虫中的作用尚不清楚。在本研究中，我们调查了刚地弓形虫速殖子在小鼠小胶质细胞培养物中的增殖情况。刚地弓形虫在这些细胞中易于增殖；当用γ干扰素加脂多糖激活小胶质细胞时，增殖受到抑制，这种处理还会上调一氧化氮（NO）合酶活性。用激活信号和NO合酶抑制剂NG-单甲基-L-精氨酸（NGMA）同时处理小胶质细胞培养物可阻止抗弓形虫活性。透射电子显微镜分析显示，活化的小胶质细胞中有退化的速殖子，而对照或NGMA组中则没有。这些发现支持这样一种观点，即活化的小胶质细胞对刚地弓形虫的宿主防御功能涉及自由基NO的产生。