Interleukin-2-dependent augmentation of the anti-tnp antibody production by sodium butyrate in cultured murine splenic b cells

Yamamoto, Ichiro; Adachi, Tomiro; Kishiro, Yumiko; Fujiwara, Masami; Gohda, Eiichi

doi:10.1016/s0192-0561(97)00036-2

Cited by 11 publications

(9 citation statements)

References 18 publications

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“…7,[17][18][19] Butyrate is an inhibitor of histone deacetylases 13,14 and causes histone hyperacetylation. 20,21 In fact, histone acetylation was reported to play a role in the augmented responsiveness of mouse B cells to LPS by butyrate.…”

Section: Discussionmentioning

confidence: 99%

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

Morikawa¹,

Sugiyama²,

Koide³

et al. 2004

J. Endotoxin Res.

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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.

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Section: Discussionmentioning

confidence: 99%

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

Morikawa¹,

Sugiyama²,

Koide³

et al. 2004

J. Endotoxin Res.

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show abstract

“…Butyrate seems to be an important bacterial modulator of NO production in macrophages. Butyrate is already known to modulate various immune functions, such as the production of colony-forming factor, 7 interleukin-8, 6 prostaglandin E 2 , 5 antibody, 21,22 and tumor necrosis factor (TNF)-α. 5 Butyrate is also capable of increasing lysozyme production by monocytic cells.…”

Section: Discussionmentioning

confidence: 99%

The inhibitory action of butyrate on lipopolysaccharide-induced nitric oxide production in RAW 264.7 murine macrophage cells

Chakravortty

Koide

Kato

et al. 2000

Journal of Endotoxin Research

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The effect of butyrate, a natural bacterial product of colonic bacterial flora, on lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW 264.7 murine macrophage cells was studied. Butyrate significantly reduced NO production in LPS-stimulated RAW cells. The inhibition was abolished by the removal of butyrate. Butyrate also inhibited the expression of inducible type NO synthase (iNOS) in LPS-stimulated RAW cells. Furthermore, butyrate prevented the activation of nuclear factor (NF)-kappaB through the stabilization of IkappaB-alpha and IkappaB-beta. Butyrate did not affect the phosphorylation of mitogen-activated protein (MAP) kinases by LPS. It was, therefore, suggested that butyrate down-regulated LPS-induced NO production in RAW cells through preventing the expression of iNOS, and that it was due to the inhibitory action of butyrate on the activation of NF-kappaB.

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“…There are several reports on the enhancing effect of butyrate on the cell function of various cell types. 7,[17][18][19] Butyrate is an inhibitor of histone deacetylases 13,14 and causes histone hyperacetylation. 20,21 In fact, histone acetylation was reported to play a role in the augmented responsiveness of mouse B cells to LPS by butyrate.…”

Section: Discussionmentioning

confidence: 99%

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

Morikawa

Sugiyama

Koide

et al. 2004

Journal of Endotoxin Research

View full text Add to dashboard Cite

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-g and/or LPS was studied. Butyrate significantly augmented NO production in END-D cells in response to IFN-g or IFN-g + LPS, but not LPS alone. The NO production was augmented by the addition of butyrate until 6 h after the stimulation with IFN-g or IFN-g + 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)-kB, mitogen-activated protein (MAP) kinases and Janus tyrosine kinase. The putative mechanism of butyrate-induced augmentation of NO production in response to IFN-g or IFN-g + LPS is discussed.

show abstract

Interleukin-2-dependent augmentation of the anti-tnp antibody production by sodium butyrate in cultured murine splenic b cells

Cited by 11 publications

References 18 publications

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

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

The inhibitory action of butyrate on lipopolysaccharide-induced nitric oxide production in RAW 264.7 murine macrophage cells

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

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