Autocrine interferon-beta stimulation augments nitric oxide production by mouse macrophage J774A.1 cells infected with herpes simplex virus type 1
| Autor: | Masashi Kurimoto, Kunihiro Ohashi, Noboru Fujioka, Masao Ikeda |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Lipopolysaccharides
Lipopolysaccharide viruses medicine.medical_treatment Immunology Herpesvirus 1 Human Biology medicine.disease_cause Nitric Oxide Microbiology Virus Antibodies Dexamethasone Nitric oxide Cell Line chemistry.chemical_compound Mice Virology medicine Macrophage Animals Autocrine signalling Macrophages Interferon-beta Cytokine Herpes simplex virus chemistry Cell culture |
| Zdroj: | Microbiology and immunology. 44(4) |
| ISSN: | 0385-5600 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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