Induction of interferon-induced transmembrane protein 3 gene expression by lipopolysaccharide in astrocytes

Akira Nakajima, Daisuke Ibi, Taku Nagai, Shinnosuke Yamada, Toshitaka Nabeshima, Kiyofumi Yamada

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Astrocytes are important modulators of the immune and inflammatory reactions in the central nervous system. We have recently demonstrated the role of interferon-induced transmembrane protein 3 (IFITM3) in long-lasting neuronal impairments in mice following neonatal immune challenge by injections of the double-stranded RNA analog polyriboinosinic polyribocytidylic acid. Here, we show that IFITM3 is induced after lipopolysaccharide (LPS) treatment in cultured astrocytes. The induction of IFITM3 by LPS was completely suppressed by the addition of anti-interferon-β (IFN-β) antibody. In addition, neutralization of tumor necrosis factor-α (TNF-α) with its antibody partially inhibited the induction of IFITM3, suggesting that LPS induces IFITM3 through autocrine secretion of IFN-β and TNF-α. Furthermore, experiments using pharmacological inhibitors suggest that LPS induces IFITM3 through activation of TANK-binding kinase 1, p38 mitogen-activated protein kinase, and nuclear factor-κB pathways. Together, these findings may provide new insight into the role of IFITM3 in the pathogenesis of neurodevelopmental diseases associated with immune activation.

Original languageEnglish
Pages (from-to)166-175
Number of pages10
JournalEuropean Journal of Pharmacology
Volume745
DOIs
Publication statusPublished - 15-12-2014
Externally publishedYes

Fingerprint

Astrocytes
Interferons
Lipopolysaccharides
Gene Expression
Proteins
Tumor Necrosis Factor-alpha
Double-Stranded RNA
p38 Mitogen-Activated Protein Kinases
Anti-Idiotypic Antibodies
Phosphotransferases
Central Nervous System
Pharmacology
Injections
Antibodies

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

Nakajima, Akira ; Ibi, Daisuke ; Nagai, Taku ; Yamada, Shinnosuke ; Nabeshima, Toshitaka ; Yamada, Kiyofumi. / Induction of interferon-induced transmembrane protein 3 gene expression by lipopolysaccharide in astrocytes. In: European Journal of Pharmacology. 2014 ; Vol. 745. pp. 166-175.
@article{69b45516ded94ac0a1ac4b7e35207b5a,
title = "Induction of interferon-induced transmembrane protein 3 gene expression by lipopolysaccharide in astrocytes",
abstract = "Astrocytes are important modulators of the immune and inflammatory reactions in the central nervous system. We have recently demonstrated the role of interferon-induced transmembrane protein 3 (IFITM3) in long-lasting neuronal impairments in mice following neonatal immune challenge by injections of the double-stranded RNA analog polyriboinosinic polyribocytidylic acid. Here, we show that IFITM3 is induced after lipopolysaccharide (LPS) treatment in cultured astrocytes. The induction of IFITM3 by LPS was completely suppressed by the addition of anti-interferon-β (IFN-β) antibody. In addition, neutralization of tumor necrosis factor-α (TNF-α) with its antibody partially inhibited the induction of IFITM3, suggesting that LPS induces IFITM3 through autocrine secretion of IFN-β and TNF-α. Furthermore, experiments using pharmacological inhibitors suggest that LPS induces IFITM3 through activation of TANK-binding kinase 1, p38 mitogen-activated protein kinase, and nuclear factor-κB pathways. Together, these findings may provide new insight into the role of IFITM3 in the pathogenesis of neurodevelopmental diseases associated with immune activation.",
author = "Akira Nakajima and Daisuke Ibi and Taku Nagai and Shinnosuke Yamada and Toshitaka Nabeshima and Kiyofumi Yamada",
year = "2014",
month = "12",
day = "15",
doi = "10.1016/j.ejphar.2014.08.034",
language = "English",
volume = "745",
pages = "166--175",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",

}

Induction of interferon-induced transmembrane protein 3 gene expression by lipopolysaccharide in astrocytes. / Nakajima, Akira; Ibi, Daisuke; Nagai, Taku; Yamada, Shinnosuke; Nabeshima, Toshitaka; Yamada, Kiyofumi.

In: European Journal of Pharmacology, Vol. 745, 15.12.2014, p. 166-175.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Induction of interferon-induced transmembrane protein 3 gene expression by lipopolysaccharide in astrocytes

AU - Nakajima, Akira

AU - Ibi, Daisuke

AU - Nagai, Taku

AU - Yamada, Shinnosuke

AU - Nabeshima, Toshitaka

AU - Yamada, Kiyofumi

PY - 2014/12/15

Y1 - 2014/12/15

N2 - Astrocytes are important modulators of the immune and inflammatory reactions in the central nervous system. We have recently demonstrated the role of interferon-induced transmembrane protein 3 (IFITM3) in long-lasting neuronal impairments in mice following neonatal immune challenge by injections of the double-stranded RNA analog polyriboinosinic polyribocytidylic acid. Here, we show that IFITM3 is induced after lipopolysaccharide (LPS) treatment in cultured astrocytes. The induction of IFITM3 by LPS was completely suppressed by the addition of anti-interferon-β (IFN-β) antibody. In addition, neutralization of tumor necrosis factor-α (TNF-α) with its antibody partially inhibited the induction of IFITM3, suggesting that LPS induces IFITM3 through autocrine secretion of IFN-β and TNF-α. Furthermore, experiments using pharmacological inhibitors suggest that LPS induces IFITM3 through activation of TANK-binding kinase 1, p38 mitogen-activated protein kinase, and nuclear factor-κB pathways. Together, these findings may provide new insight into the role of IFITM3 in the pathogenesis of neurodevelopmental diseases associated with immune activation.

AB - Astrocytes are important modulators of the immune and inflammatory reactions in the central nervous system. We have recently demonstrated the role of interferon-induced transmembrane protein 3 (IFITM3) in long-lasting neuronal impairments in mice following neonatal immune challenge by injections of the double-stranded RNA analog polyriboinosinic polyribocytidylic acid. Here, we show that IFITM3 is induced after lipopolysaccharide (LPS) treatment in cultured astrocytes. The induction of IFITM3 by LPS was completely suppressed by the addition of anti-interferon-β (IFN-β) antibody. In addition, neutralization of tumor necrosis factor-α (TNF-α) with its antibody partially inhibited the induction of IFITM3, suggesting that LPS induces IFITM3 through autocrine secretion of IFN-β and TNF-α. Furthermore, experiments using pharmacological inhibitors suggest that LPS induces IFITM3 through activation of TANK-binding kinase 1, p38 mitogen-activated protein kinase, and nuclear factor-κB pathways. Together, these findings may provide new insight into the role of IFITM3 in the pathogenesis of neurodevelopmental diseases associated with immune activation.

UR - http://www.scopus.com/inward/record.url?scp=84918826872&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84918826872&partnerID=8YFLogxK

U2 - 10.1016/j.ejphar.2014.08.034

DO - 10.1016/j.ejphar.2014.08.034

M3 - Article

VL - 745

SP - 166

EP - 175

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

ER -