Up-regulation of indoleamine 2,3-dioxygenase by lipopolysaccharide is regulated through activation of p38 mitogen-activated protein kinase and nuclear factor-κB

Suwako Fujigaki, Kanako Takahashi, Hidetsugu Fujigaki, Masao Takemura, Mitsuru Seishima, Kuniaki Saito

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Indoleamine 2,3-dioxygenase (IDO) is up-regulated by interferon-γ (IFN-γ)-dependent and/or -independent mechanisms. IFN-γ-dependent mechanism is regulated through signal transducer and activator of transcription 1α (STAT1α) and interferon regulatory factor 1 (IRF-1). On the other hand, IFN-γ-independent mechanism of IDO induction has not been identified. In this study, we explored whether IDO induction by LPS requires the STAT1α and IRF-1 signaling pathways. IDO was induced by LPS or IFN-γ in THP-1 cells and a synergistic IDO induction occurred in THP-1 cultured with a combination of tumor necrosis factor-α, interleukin-6 and interleukin-1β. An electrophoretic mobility shift assay using STAT1α and IRF-1 consensus oligonucleotide probes showed no STAT1α or IRF-1 binding activities in LPS-stimulated THP-1 cells. Further, the LPS-induced IDO activity was inhibited by both p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) inhibitors. These results suggest that IDO induction by LPS is not regulated through the STAT1α or IRF-1 binding activities that are induced by IFN-γ, and may be related to the activity of the p38 MAPK pathway and/or NF-κB.

Original languageEnglish
Pages (from-to)200-204
Number of pages5
JournalInternational Congress Series
Volume1304
DOIs
Publication statusPublished - 01-11-2007
Externally publishedYes

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Indoleamine-Pyrrole 2,3,-Dioxygenase
p38 Mitogen-Activated Protein Kinases
Interferon Regulatory Factor-1
STAT1 Transcription Factor
Lipopolysaccharides
Up-Regulation
Interferons
Oligonucleotide Probes
Electrophoretic Mobility Shift Assay
Interleukin-1
Interleukin-6
Tumor Necrosis Factor-alpha

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

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title = "Up-regulation of indoleamine 2,3-dioxygenase by lipopolysaccharide is regulated through activation of p38 mitogen-activated protein kinase and nuclear factor-κB",
abstract = "Indoleamine 2,3-dioxygenase (IDO) is up-regulated by interferon-γ (IFN-γ)-dependent and/or -independent mechanisms. IFN-γ-dependent mechanism is regulated through signal transducer and activator of transcription 1α (STAT1α) and interferon regulatory factor 1 (IRF-1). On the other hand, IFN-γ-independent mechanism of IDO induction has not been identified. In this study, we explored whether IDO induction by LPS requires the STAT1α and IRF-1 signaling pathways. IDO was induced by LPS or IFN-γ in THP-1 cells and a synergistic IDO induction occurred in THP-1 cultured with a combination of tumor necrosis factor-α, interleukin-6 and interleukin-1β. An electrophoretic mobility shift assay using STAT1α and IRF-1 consensus oligonucleotide probes showed no STAT1α or IRF-1 binding activities in LPS-stimulated THP-1 cells. Further, the LPS-induced IDO activity was inhibited by both p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) inhibitors. These results suggest that IDO induction by LPS is not regulated through the STAT1α or IRF-1 binding activities that are induced by IFN-γ, and may be related to the activity of the p38 MAPK pathway and/or NF-κB.",
author = "Suwako Fujigaki and Kanako Takahashi and Hidetsugu Fujigaki and Masao Takemura and Mitsuru Seishima and Kuniaki Saito",
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Up-regulation of indoleamine 2,3-dioxygenase by lipopolysaccharide is regulated through activation of p38 mitogen-activated protein kinase and nuclear factor-κB. / Fujigaki, Suwako; Takahashi, Kanako; Fujigaki, Hidetsugu; Takemura, Masao; Seishima, Mitsuru; Saito, Kuniaki.

In: International Congress Series, Vol. 1304, 01.11.2007, p. 200-204.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Up-regulation of indoleamine 2,3-dioxygenase by lipopolysaccharide is regulated through activation of p38 mitogen-activated protein kinase and nuclear factor-κB

AU - Fujigaki, Suwako

AU - Takahashi, Kanako

AU - Fujigaki, Hidetsugu

AU - Takemura, Masao

AU - Seishima, Mitsuru

AU - Saito, Kuniaki

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Y1 - 2007/11/1

N2 - Indoleamine 2,3-dioxygenase (IDO) is up-regulated by interferon-γ (IFN-γ)-dependent and/or -independent mechanisms. IFN-γ-dependent mechanism is regulated through signal transducer and activator of transcription 1α (STAT1α) and interferon regulatory factor 1 (IRF-1). On the other hand, IFN-γ-independent mechanism of IDO induction has not been identified. In this study, we explored whether IDO induction by LPS requires the STAT1α and IRF-1 signaling pathways. IDO was induced by LPS or IFN-γ in THP-1 cells and a synergistic IDO induction occurred in THP-1 cultured with a combination of tumor necrosis factor-α, interleukin-6 and interleukin-1β. An electrophoretic mobility shift assay using STAT1α and IRF-1 consensus oligonucleotide probes showed no STAT1α or IRF-1 binding activities in LPS-stimulated THP-1 cells. Further, the LPS-induced IDO activity was inhibited by both p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) inhibitors. These results suggest that IDO induction by LPS is not regulated through the STAT1α or IRF-1 binding activities that are induced by IFN-γ, and may be related to the activity of the p38 MAPK pathway and/or NF-κB.

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