Ito Hiroyasu, Koide Naoki, Morikawa Akiko, Hassan Ferdaus, Islam Shamima, Tumurkhuu Gantsetseg, Mori Isamu, Yoshida Tomoaki, Kakumu Shinichi, Moriwaki Hisataka, Yokochi Takashi
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan.
J Endotoxin Res. 2005;11(4):213-9. doi: 10.1179/096805105X46628.
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.
研究了α-半乳糖神经酰胺（α-GalCer）对脂多糖（LPS）诱导的小鼠腹腔细胞中一氧化氮（NO）产生的影响。α-GalCer增强了LPS诱导的小鼠腹腔细胞中NO的产生，但对RAW 264.7巨噬细胞无此作用。α-GalCer增强了LPS刺激的腹腔细胞中NO的产生，但未增强肿瘤坏死因子（TNF）-α的产生。腹腔细胞对α-GalCer产生显著水平的干扰素（IFN）-γ，抗IFN-γ抗体消除了α-GalCer对LPS诱导的NO产生的增强作用。此外，抗IFN-γ抗体阻止了α-GalCer诱导的诱导型一氧化氮合酶mRNA表达增强。α-GalCer在自然杀伤T（NKT）缺陷小鼠的腹腔细胞中未增强LPS诱导的NO产生。因此，提示α-GalCer可能通过NKT细胞释放IFN-γ来增强LPS诱导的腹腔细胞中NO的产生。
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