Autocrine interferon-beta stimulation augments nitric oxide production by mouse macrophage J774A.1 cells infected with herpes simplex virus type 1.
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.
Fujioka
N
N
Fujisaki Institute, Hayashibara Biochemical Laboratories, Inc., Okayama, Okayama, Japan.
Ohashi
K
K
Ikeda
M
M
Kurimoto
M
M
D000818:Animals; D000906:Antibodies / Q000276:immunology; D002460:Cell Line; D003907:Dexamethasone / Q000494:pharmacology; D018259:Herpesvirus 1, Human / Q000502:physiology*; D016899:Interferon-beta / Q000276:immunology / Q000494:pharmacology / Q000502:physiology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism / Q000821:virology*; D051379:Mice; D009569:Nitric Oxide / Q000096:biosynthesis*
D000906:Antibodies; D008070:Lipopolysaccharides; D009569:Nitric Oxide; D016899:Interferon-beta; D003907:Dexamethasone