Autocrine Interferon-β Stimulation Augments Nitric Oxide Production by Mouse Macrophage J774A.1 Cells Infected with Herpes Simplex Virus Type 1

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)-β treatment. These results suggest that autocrine IFN-β plays a role in NO release by J774A.1 cells stimulated with HSV-1 or LPS.