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Journal of Endotoxin Research
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Augmentation of lipopolysaccharide-induced nitric oxide production by {alpha}-galactosylceramide in mouse peritoneal cells

Hiroyasu Ito

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

Naoki Koide

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

Akiko Morikawa

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

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

Shinichi Kakumu

Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Hisataka Moriwaki

First Department of Internal Medicine, Gifu University School of Medicine, Gifu, Japan

Takashi Yokochi

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

The effect of {alpha}-galactosylceramide ({alpha}-GalCer) on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in mouse peritoneal cells was studied. {alpha}-GalCer augmented LPS-induced NO production in mouse peritoneal cells, but not in RAW 264.7 macrophage cells. {alpha}-GalCer augmented NO production, but not tumor necrosis factor (TNF)-{alpha} production in LPS-stimulated peritoneal cells. Peritoneal cells produced a significant level of interferon (IFN)-{gamma} in response to {alpha}-GalCer and anti-IFN-{gamma} antibody abolished the augmentation of LPS-induced NO production by {alpha}-GalCer. Moreover, anti-IFN-{gamma} antibody prevented the enhanced expression of an inducible type of NO synthase mRNA by {alpha}-GalCer. {alpha}-GalCer did not augment LPS-induced NO production in peritoneal cells from natural killer T (NKT)-deficient mice. Therefore, it was suggested that {alpha}-GalCer might augment LPS-induced NO production in peritoneal cells through release of IFN-{gamma} from NKT cells.

Key Words: {alpha}-Galactosylceramide • LPS • nitric oxide • peritoneal cell • NKT cell

Journal of Endotoxin Research, Vol. 11, No. 4, 213-219 (2005)
DOI: 10.1177/09680519050110040501
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