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Infection and Immunity, November 2000, p. 6209-6214, Vol. 68, No. 11
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Augmentation of Nitric Oxide Production by Gamma Interferon in a Mouse Vascular Endothelial Cell Line and Its Modulation by Tumor Necrosis Factor Alpha and Lipopolysaccharide

Akiko Morikawa, Naoki Koide, Yutaka Kato, Tsuyoshi Sugiyama, Dipshikha Chakravortty, Tomoaki Yoshida, and Takashi Yokochi*

Department of Microbiology and Immunology and Division of Bacterial Toxins, Research Center for Infectious Diseases, Aichi Medical University, Nagakute, Aichi 480-1195, Japan

Received 13 March 2000/Returned for modification 10 July 2000/Accepted 11 August 2000

The effect of gamma interferon (IFN-gamma ), tumor necrosis factor alpha (TNF-alpha ), and lipopolysaccharide (LPS) on nitric oxide (NO) production in the mouse vascular aortic endothelial cell line END-D was examined. LPS, TNF-alpha , and a low concentration of IFN-gamma inhibited NO production in END-D cells, while a high concentration of IFN-gamma definitely enhanced it. The NO production induced by a high concentration of IFN-gamma was further augmented by using IFN-gamma in combination with LPS or TNF-alpha . In sequential incubations of LPS and IFN-gamma , the enhancement of NO production required prior treatment with IFN-gamma . Stimulation of END-D cells with a high concentration of IFN-gamma led to the expression of inducible NO synthase (iNOS). The augmentation of NO production by IFN-gamma alone or in combination with LPS or TNF-alpha was completely blocked by several inhibitors of iNOS. It was strongly suggested that a high concentration of IFN-gamma itself enhanced NO production in END-D cells through inducing the expression of iNOS. LPS and TNF-alpha exclusively modulated the activity of iNOS once its expression was triggered by IFN-gamma . On the other hand, a low concentration of IFN-gamma , LPS, and TNF-alpha reduced NO production through down-regulating constitutive NOS (cNOS). The differential regulation of cNOS- and iNOS-mediated NO production by IFN-gamma , TNF-alpha , and LPS is discussed.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Aichi Medical University, Nagakute, Aichi 480-1195, Japan. Phone: 81-561-62-3311, ext. 2269. Fax: 81-561-63-9187. E-mail: yokochi{at}aichi-med-u.ac.jp.

Infection and Immunity, November 2000, p. 6209-6214, Vol. 68, No. 11
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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