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

被引：16

作者：

Ito, H ^{[1
]}

Koide, N

Morikawa, A

Hassan, F

Islam, S

Tumurkhuu, G

Mori, I

Yoshida, T

Kakumu, S

Moriwaki, H

Yokochi, T

机构：

[1] Aichi Med Univ, Sch Med, Dept Microbiol & Immunol, Aichi 4801195, Japan

[2] Aichi Med Univ, Sch Med, Dept Internal Med, Aichi 4801195, Japan

[3] Gifu Univ, Sch Med, Dept Internal Med 1, Gifu 500, Japan

来源：

JOURNAL OF ENDOTOXIN RESEARCH | 2005年 / 11卷 / 04期

关键词：

alpha-galactosylceramide; LPS; nitric oxide; peritoneal cell; NKT cell;

D O I：

10.1179/096805105X46628

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

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.

引用

页码：213 / 219

页数：7

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