TY - JOUR
T1 - Augmentation of lipopolysaccharide-induced nitric oxide production byα-galactosylceramide in mouse peritoneal cells
AU - Ito, Hiroyasu
AU - Koide, Naoki
AU - Morikawa, Akiko
AU - Hassan, Ferdaus
AU - Islam, Shamima
AU - Tumurkhuu, Gantsetseg
AU - Mori, Isamu
AU - Yoshida, Tomoaki
AU - Kakumu, Shinichi
AU - Moriwaki, Hisataka
AU - Yokochi, Takashi
PY - 2005
Y1 - 2005
N2 - 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.
AB - 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.
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U2 - 10.1179/096805105X46628
DO - 10.1179/096805105X46628
M3 - Article
C2 - 16176657
AN - SCOPUS:25444434850
SN - 0968-0519
VL - 11
SP - 213
EP - 219
JO - Journal of Endotoxin Research
JF - Journal of Endotoxin Research
IS - 4
ER -
