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Journal of Endotoxin Research
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Lipopolysaccharide enhances interferon-{gamma}-induced nitric oxide (NO) production in murine vascular endothelial cells via augmentation of interferon regulatory factor-1 activation

Naoki Koide

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan, koide{at}aichi-med-u.ac.jp

Mya Mya Mu

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Ferdaus Hassan

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Shamima Islam

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Gantsetseg Tumurkhuu

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Jargalsaikhan Dagvadorj

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Yoshikazu Naiki

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Isamu Mori

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Tomoaki Yoshida

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Takashi Yokochi

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Lipopolysaccharide (LPS) enhances the production of nitric oxide (NO) in interferon (IFN)-{gamma}stimulated vascular endothelial cells. We studied the mechanism by which LPS enhances IFN-{gamma}-induced NO production by using the murine vascular endothelial cell line, END-D. LPS enhanced IFN-{gamma}induced NO production via augmented expression of inducible type NO synthase (iNOS) mRNA. LPS significantly augmented the activation of interferon regulatory factor (IRF)-1 in IFN-{gamma}-stimulated END-D cells, although it did not affect the activation of either MyD88-dependent nuclear factor (NF)-{kappa}B or MyD88-independent IRF-3. SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), prevented the nuclear translocation of IRF-1 in LPS and IFN-{gamma}-stimulated END-D cells, and inhibited the iNOS expression and NO production in those cells. Therefore, it is proposed that LPS enhanced NO production in IFN-{gamma}-stimulated END-D cells via augmenting p38 MAPKmediated IRF-1 activation.

Key Words: LPS • interferon-{gamma} • nitric oxide • vascular endothelial cell • IRF-1

Journal of Endotoxin Research, Vol. 13, No. 3, 167-175 (2007)
DOI: 10.1177/0968051907080894
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