title: Autocrine interferon-beta 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)-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.
authors.affiliation: Fujisaki Institute, Hayashibara Biochemical Laboratories, Inc., Okayama, Okayama, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Fujioka
authors.forename: K
authors.initials: K
authors.lastname: Ohashi
authors.forename: M
authors.initials: M
authors.lastname: Ikeda
authors.forename: M
authors.initials: M
authors.lastname: Kurimoto
mesh_terms: 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*
chemical_list: D000906:Antibodies; D008070:Lipopolysaccharides; D009569:Nitric Oxide; D016899:Interferon-beta; D003907:Dexamethasone