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

Augmentation of lipopolysaccharide-induced nitric oxide production by α-galactosylceramide in mouse peritoneal cells