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Butyrate enhances the production of nitric oxide in mouse vascular endothelial cells in response to gamma interferon

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Tsuyoshi Sugiyama

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Naoki Koide

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Isamu Mori

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Mya Mya Mu

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Tomoaki Yoshida

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan, yokochi{at}aichi-med-u.ac.jp

Ferdaus Hassan

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Shamima Islam

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

Takashi Yokochi

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan

The effect of butyrate, a natural bacterial product of colonic bacterial flora, on nitric oxide (NO) production in murine vascular endothelial cell line END-D in response to IFN- and/or LPS was studied. Butyrate significantly augmented NO production in END-D cells in response to IFN- or IFN- + LPS, but not LPS alone. The NO production was augmented by the addition of butyrate until 6 h after the stimulation with IFN- or IFN- + LPS. The augmentation was abolished by the removal of butyrate from the cultures. Butyrate enhanced the expression of inducible type NO synthase (iNOS) in the stimulated END-D cells. Furthermore, butyrate-enhanced NO production in the presence of various signal inhibitors down-regulating the signal pathways using nuclear factor (NF)-B, mitogen-activated protein (MAP) kinases and Janus tyrosine kinase. The putative mechanism of butyrate-induced augmentation of NO production in response to IFN- or IFN- + LPS is discussed.

Key Words: Butyrate • nitric oxide • mouse vascular endothelial cells • IFN-

Journal of Endotoxin Research, Vol. 10, No. 1, 33-38 (2004)
DOI: 10.1177/09680519040100010401


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