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Autocrine interferon-beta stimulation augments nitric oxide production by mouse macrophage J774A.1 cells infected
1Fujisaki Institute, Hayashibara Biochemical Laboratories, Inc., Okayama, Okayama, Japan.
Microbiology and Immunology
|June 1, 2000
Abstract:
The pathogenic roles of nitric oxide (NO) in 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.