Morikawa Akiko, Sugiyama Tsuyoshi, Koide Naoki, Mori Isamu, Mu Mya Mya, Yoshida Tomoaki, Hassan Ferdaus, Islam Shamima, Yokochi Takashi
Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Nagakute, Aichi, Japan.
J Endotoxin Res. 2004;10(1):32-8. doi: 10.1179/096805104225003852.
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-gamma and/or LPS was studied. Butyrate significantly augmented NO production in END-D cells in response to IFN-gamma or IFN-gamma + LPS, but not LPS alone. The NO production was augmented by the addition of butyrate until 6 h after the stimulation with IFN-gamma or IFN-gamma + 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)-kappaB, mitogen-activated protein (MAP) kinases and Janus tyrosine kinase. The putative mechanism of butyrate-induced augmentation of NO production in response to IFN-gamma or IFN-gamma + LPS is discussed.
