Hirofumi Ohtaki, Hiroyasu Ito, Kazuki Ando, Tetsuya Ishikawa, Masato Hoshi, Ryo Tanaka, Yosuke Osawa, Takashi Yokochi, Hisataka Moriwaki, Kuniaki Saito, Mitsuru Seishima
Department of Informative Clinical Medicine, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu 501-1194, Japan.
Biochemical and biophysical research communications 2009 Nov 13In this study, we demonstrated that lipopolysaccharide (LPS) markedly increased nitric oxide (NO) production and indoleamine 2,3-dioxygenase (IDO) activity in mouse peritoneal cells in the presence of activated Valpha14 natural killer T cells. Moreover, LPS-induced NO production in peritoneal cells from IDO-knockout (KO) mice was more increased than that from wild-type mice. However, there was no significant difference in the expression of inducible nitric oxide synthase (iNOS) mRNA and protein between the wild-type and IDO-KO mice. No significant difference was also observed in the ratio of CD3- and DX5-positive cells and F4/80- and TLR4-positive cells in peritoneal cells between the wild-type and IDO-KO mice. Since the IDO activity was enhanced by an NO inhibitor, NO may be post-translationally consumed by inhibiting the IDO activity. IDO is well known to play an important role in immunosuppression during inflammatory disease. Therefore, the inhibition of IDO by NO may exacerbate inflammation in the peritoneal cavity.
Hirofumi Ohtaki, Hiroyasu Ito, Kazuki Ando, Tetsuya Ishikawa, Masato Hoshi, Ryo Tanaka, Yosuke Osawa, Takashi Yokochi, Hisataka Moriwaki, Kuniaki Saito, Mitsuru Seishima. Interaction between LPS-induced NO production and IDO activity in mouse peritoneal cells in the presence of activated Valpha14 NKT cells. Biochemical and biophysical research communications. 2009 Nov 13;389(2):229-34
PMID: 19715679
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