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

Hiroyasu Ito, Naoki Koide, Akiko Morikawa, Ferdaus Hassan, Shamima Islam, Gantsetseg Tumurkhuu, Isamu Mori, Tomoaki Yoshida, Shinichi Kakumu, Hisataka Moriwaki, Takashi Yokochi

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)213-219
Number of pages7
JournalJournal of Endotoxin Research
Volume11
Issue number4
DOIs
Publication statusPublished - 2005

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Molecular Biology
  • Cell Biology
  • Infectious Diseases

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