Expression of IL-27 p28 by Theiler's virus-infected macrophages depends on TLR3 and TLR7 activation of JNK-MAP-kinases

Lara Hause, Fahd M. Al-Salleeh, Thomas M Petro

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Theiler's murine encephalomyelitis virus (TMEV) causes a demyelinating disease (DD) due to infection of macrophages, stimulation of macrophage Toll-like receptor (TLR)3 and TLR7 pathways, activation of Mitogen-activated protein kinases (MAPK)s, and production of macrophages cytokines. Because expression of IL-27, a macrophage cytokine composed of p28 and EBI3 subunits, has been implicated in DD, we examined IL-27 subunit mRNA expression during TMEV infection of RAW264.7 cells, a macrophage cell line. TMEV infection of RAW264.7 cells did not affect cell viability, resulted in viral RNA replication, as well as p28 and EBI3 expression. Expression of p28 in TMEV-infected RAW264.7 cells depended on TLR3 and TLR7, as well as JNK but not p38 or ERK MAPKs. Since TMEV causes DD in SJL/J but not B10.S mice we determined the difference in expression of IL-27 subunit mRNA in SJL/J compared to B10.S macrophages. SJL/J macrophages expressed significantly more p28 mRNA after TMEV infection and after stimulation with TLR3 and TLR7 agonists compared with B10.S macrophages. Therefore, macrophages expression of IL-27 p28 mRNA in response to TMEV is due to activation of TLR3, TLR7, and JNK MAPKs pathways.

Original languageEnglish (US)
Pages (from-to)159-167
Number of pages9
JournalAntiviral Research
Volume76
Issue number2
DOIs
StatePublished - Nov 1 2007

Fingerprint

Interleukin-27
Theilovirus
MAP Kinase Kinase 4
Macrophages
Demyelinating Diseases
Virus Diseases
Messenger RNA
Toll-Like Receptor 3
Cytokines
MAP Kinase Signaling System
Viral RNA
Mitogen-Activated Protein Kinases
Cell Survival

Keywords

  • IL-27
  • JNK
  • Macrophages
  • RAW264.7 cells
  • TLR3
  • TLR7
  • TMEV

ASJC Scopus subject areas

  • Pharmacology
  • Virology

Cite this

Expression of IL-27 p28 by Theiler's virus-infected macrophages depends on TLR3 and TLR7 activation of JNK-MAP-kinases. / Hause, Lara; Al-Salleeh, Fahd M.; Petro, Thomas M.

In: Antiviral Research, Vol. 76, No. 2, 01.11.2007, p. 159-167.

Research output: Contribution to journalArticle

@article{ac8245eebb5948ecbec99a422130efeb,
title = "Expression of IL-27 p28 by Theiler's virus-infected macrophages depends on TLR3 and TLR7 activation of JNK-MAP-kinases",
abstract = "Theiler's murine encephalomyelitis virus (TMEV) causes a demyelinating disease (DD) due to infection of macrophages, stimulation of macrophage Toll-like receptor (TLR)3 and TLR7 pathways, activation of Mitogen-activated protein kinases (MAPK)s, and production of macrophages cytokines. Because expression of IL-27, a macrophage cytokine composed of p28 and EBI3 subunits, has been implicated in DD, we examined IL-27 subunit mRNA expression during TMEV infection of RAW264.7 cells, a macrophage cell line. TMEV infection of RAW264.7 cells did not affect cell viability, resulted in viral RNA replication, as well as p28 and EBI3 expression. Expression of p28 in TMEV-infected RAW264.7 cells depended on TLR3 and TLR7, as well as JNK but not p38 or ERK MAPKs. Since TMEV causes DD in SJL/J but not B10.S mice we determined the difference in expression of IL-27 subunit mRNA in SJL/J compared to B10.S macrophages. SJL/J macrophages expressed significantly more p28 mRNA after TMEV infection and after stimulation with TLR3 and TLR7 agonists compared with B10.S macrophages. Therefore, macrophages expression of IL-27 p28 mRNA in response to TMEV is due to activation of TLR3, TLR7, and JNK MAPKs pathways.",
keywords = "IL-27, JNK, Macrophages, RAW264.7 cells, TLR3, TLR7, TMEV",
author = "Lara Hause and Al-Salleeh, {Fahd M.} and Petro, {Thomas M}",
year = "2007",
month = "11",
day = "1",
doi = "10.1016/j.antiviral.2007.06.013",
language = "English (US)",
volume = "76",
pages = "159--167",
journal = "Antiviral Research",
issn = "0166-3542",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Expression of IL-27 p28 by Theiler's virus-infected macrophages depends on TLR3 and TLR7 activation of JNK-MAP-kinases

AU - Hause, Lara

AU - Al-Salleeh, Fahd M.

AU - Petro, Thomas M

PY - 2007/11/1

Y1 - 2007/11/1

N2 - Theiler's murine encephalomyelitis virus (TMEV) causes a demyelinating disease (DD) due to infection of macrophages, stimulation of macrophage Toll-like receptor (TLR)3 and TLR7 pathways, activation of Mitogen-activated protein kinases (MAPK)s, and production of macrophages cytokines. Because expression of IL-27, a macrophage cytokine composed of p28 and EBI3 subunits, has been implicated in DD, we examined IL-27 subunit mRNA expression during TMEV infection of RAW264.7 cells, a macrophage cell line. TMEV infection of RAW264.7 cells did not affect cell viability, resulted in viral RNA replication, as well as p28 and EBI3 expression. Expression of p28 in TMEV-infected RAW264.7 cells depended on TLR3 and TLR7, as well as JNK but not p38 or ERK MAPKs. Since TMEV causes DD in SJL/J but not B10.S mice we determined the difference in expression of IL-27 subunit mRNA in SJL/J compared to B10.S macrophages. SJL/J macrophages expressed significantly more p28 mRNA after TMEV infection and after stimulation with TLR3 and TLR7 agonists compared with B10.S macrophages. Therefore, macrophages expression of IL-27 p28 mRNA in response to TMEV is due to activation of TLR3, TLR7, and JNK MAPKs pathways.

AB - Theiler's murine encephalomyelitis virus (TMEV) causes a demyelinating disease (DD) due to infection of macrophages, stimulation of macrophage Toll-like receptor (TLR)3 and TLR7 pathways, activation of Mitogen-activated protein kinases (MAPK)s, and production of macrophages cytokines. Because expression of IL-27, a macrophage cytokine composed of p28 and EBI3 subunits, has been implicated in DD, we examined IL-27 subunit mRNA expression during TMEV infection of RAW264.7 cells, a macrophage cell line. TMEV infection of RAW264.7 cells did not affect cell viability, resulted in viral RNA replication, as well as p28 and EBI3 expression. Expression of p28 in TMEV-infected RAW264.7 cells depended on TLR3 and TLR7, as well as JNK but not p38 or ERK MAPKs. Since TMEV causes DD in SJL/J but not B10.S mice we determined the difference in expression of IL-27 subunit mRNA in SJL/J compared to B10.S macrophages. SJL/J macrophages expressed significantly more p28 mRNA after TMEV infection and after stimulation with TLR3 and TLR7 agonists compared with B10.S macrophages. Therefore, macrophages expression of IL-27 p28 mRNA in response to TMEV is due to activation of TLR3, TLR7, and JNK MAPKs pathways.

KW - IL-27

KW - JNK

KW - Macrophages

KW - RAW264.7 cells

KW - TLR3

KW - TLR7

KW - TMEV

UR - http://www.scopus.com/inward/record.url?scp=34548643540&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34548643540&partnerID=8YFLogxK

U2 - 10.1016/j.antiviral.2007.06.013

DO - 10.1016/j.antiviral.2007.06.013

M3 - Article

C2 - 17675254

AN - SCOPUS:34548643540

VL - 76

SP - 159

EP - 167

JO - Antiviral Research

JF - Antiviral Research

SN - 0166-3542

IS - 2

ER -