Autocrine interferon-β stimulation augments nitric oxide production by mouse macrophage J774A.1 cells infected with herpes simplex virus type 1

被引：4

作者：

Fujioka, N ^{[1
]}

Ohashi, K ^{[1
]}

Ikeda, M ^{[1
]}

Kurimoto, M ^{[1
]}

机构：

[1] Hayashibara Biochem Labs Inc, Fujisaki Inst, Okayama 7028006, Japan

来源：

MICROBIOLOGY AND IMMUNOLOGY | 2000年 / 44卷 / 04期

关键词：

HSV-1; LPS; NO; IFN;

D O I：

10.1111/j.1348-0421.2000.tb02497.x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The pathogenic roles of nitric oxide (NO) ire mouse models have been reported for herpes simplex virus type 1 (HSV-1)-induced pneumonia as well as endotoxin shock. We compared the mechanism of NO production induced by HSV-1 with that induced by lipopolysaccharide (LPS) using a mouse macrophage cell line, J774A.1. Both HSV-1 and LPS induced NO production as well as antiviral activity, which were attenuated by anti-interferon (IFN)-beta treatment. These results suggest that autocrine IFN-beta plays a role in NO release by J774A.1 cells stimulated with HSV-1 or LPS.

引用

页码：283 / 287

页数：5

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