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  • Title: Valpha14 NKT cells activated by alpha-galactosylceramide augment lipopolysaccharide-induced nitric oxide production in mouse intra-hepatic lymphocytes.
    Author: Ohtaki H, Ito H, Ando K, Ishikawa T, Saito K, Imawari M, Yokochi T, Moriwaki H, Seishima M.
    Journal: Biochem Biophys Res Commun; 2009 Jan 16; 378(3):579-83. PubMed ID: 19056341.
    Abstract:
    Valpha14 natural killer T (Valpha14 NKT) cells activated by alpha-galactosylceramide (alpha-GalCer) secrete a large amount of Th1 and Th2 cytokines. IFN-gamma plays a crucial role in the inflammation response, and is also known as an activator of nitric oxide (NO) production. We previously reported that lipopolysaccharide (LPS)-induced NO production is augmented by alpha-GalCer in mouse peritoneal cells. Since the liver is susceptible to LPS stimulation via the portal vein, we examined the effect of alpha-GalCer on LPS-induced NO production in murine intra-hepatic lymphocytes (IHLs). Although IHLs augmented LPS-induced NO production by alpha-GalCer administration, such an augmentation was not observed in non-treated mice. Furthermore, alpha-GalCer did not augment LPS-induced NO production in IHLs from IFN-gamma knockout mice. In flow cytometry analysis of IHLs from alpha-GalCer-treated mice, the ratio and number of F4/80- and TLR4-positive cells rose as compared with non-treated mice. The liver injury may be induced by LPS and NO under the condition where Valpha14 NKT cells were activated.
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