Interleukin-1β stimulates macrophage inflammatory protein-1α and -1β expression in human neuronal cells (NT2-N)

Chang Jiang Guo, Steven D. Douglas, Jian Ping Lai, David E Pleasure, Yuan Li, Marge Williams, Peter Bannerman, Li Song, Wen Zhe Ho

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

Chemokines are important mediators in immune responses and inflammatory processes of neuroimmunologic and infectious diseases. Although chemokines are expressed predominantly by cells of the immune system, neurons also express chemokines and chemokine receptors. We report herein that human neuronal cells (NT2-N) produce macrophage inflammatory protein-1α and -1β (MIP-1α and MIP-1β), which could be enhanced by interleukin (IL)-1β at both mRNA and protein levels. The addition of supernatants from human peripheral blood monocyte-derived macrophage (MDM) cultures Induced MIP-1β mRNA expression in NT2-N cells. Anti-IL-1β antibody removed most, but not all, of the MDM culture supernatant-induced MIP-1β mRNA expression in NT2-N cells, suggesting that IL-1β in the MDM culture supernatants is a major factor in the induction of MIP-1β expression. Investigation of the mechanism(s) responsible for IL-1β-induced MIP-1α and -1β expression demonstrated that IL-1β activated nuclear factor kappa B (NF-κB) promoter-directed luciferase activity in NT2-N cells. Caffeic acid phenethyl ester, a potent and specific inhibitor of activation of NF-κB, not only blocked IL-1β-induced activation of the NF-κB promoter but also decreased IL-1β-induced MIP-1α and -1β expression in NT2-N cells. These data suggest that NF-κB is at least partially involved in the IL-1β-mediated action on MIP-1α and -1β in NT2-N cells. IL-1β-mediated up-regulation of β-chemokine expression may have important implications in the immunopathogenesis of inflammatory diseases in the CNS.

Original languageEnglish (US)
Pages (from-to)997-1005
Number of pages9
JournalJournal of Neurochemistry
Volume84
Issue number5
DOIs
StatePublished - Mar 2003
Externally publishedYes

Fingerprint

Macrophage Inflammatory Proteins
Interleukin-1
NF-kappa B
Chemokines
Macrophages
Cell culture
Messenger RNA
Chemical activation
Chemokine Receptors
Immune system
Central Nervous System Diseases
Luciferases
Neurons
Communicable Diseases
Immune System
Blood
Up-Regulation

Keywords

  • β-chemokines
  • Interleukin-1β
  • Macrophage inflammatory protein-1α
  • Macrophage inflammatory protein-1β
  • NT2-N
  • Nuclear factor-κB

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

Interleukin-1β stimulates macrophage inflammatory protein-1α and -1β expression in human neuronal cells (NT2-N). / Guo, Chang Jiang; Douglas, Steven D.; Lai, Jian Ping; Pleasure, David E; Li, Yuan; Williams, Marge; Bannerman, Peter; Song, Li; Ho, Wen Zhe.

In: Journal of Neurochemistry, Vol. 84, No. 5, 03.2003, p. 997-1005.

Research output: Contribution to journalArticle

Guo, Chang Jiang ; Douglas, Steven D. ; Lai, Jian Ping ; Pleasure, David E ; Li, Yuan ; Williams, Marge ; Bannerman, Peter ; Song, Li ; Ho, Wen Zhe. / Interleukin-1β stimulates macrophage inflammatory protein-1α and -1β expression in human neuronal cells (NT2-N). In: Journal of Neurochemistry. 2003 ; Vol. 84, No. 5. pp. 997-1005.
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T1 - Interleukin-1β stimulates macrophage inflammatory protein-1α and -1β expression in human neuronal cells (NT2-N)

AU - Guo, Chang Jiang

AU - Douglas, Steven D.

AU - Lai, Jian Ping

AU - Pleasure, David E

AU - Li, Yuan

AU - Williams, Marge

AU - Bannerman, Peter

AU - Song, Li

AU - Ho, Wen Zhe

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N2 - Chemokines are important mediators in immune responses and inflammatory processes of neuroimmunologic and infectious diseases. Although chemokines are expressed predominantly by cells of the immune system, neurons also express chemokines and chemokine receptors. We report herein that human neuronal cells (NT2-N) produce macrophage inflammatory protein-1α and -1β (MIP-1α and MIP-1β), which could be enhanced by interleukin (IL)-1β at both mRNA and protein levels. The addition of supernatants from human peripheral blood monocyte-derived macrophage (MDM) cultures Induced MIP-1β mRNA expression in NT2-N cells. Anti-IL-1β antibody removed most, but not all, of the MDM culture supernatant-induced MIP-1β mRNA expression in NT2-N cells, suggesting that IL-1β in the MDM culture supernatants is a major factor in the induction of MIP-1β expression. Investigation of the mechanism(s) responsible for IL-1β-induced MIP-1α and -1β expression demonstrated that IL-1β activated nuclear factor kappa B (NF-κB) promoter-directed luciferase activity in NT2-N cells. Caffeic acid phenethyl ester, a potent and specific inhibitor of activation of NF-κB, not only blocked IL-1β-induced activation of the NF-κB promoter but also decreased IL-1β-induced MIP-1α and -1β expression in NT2-N cells. These data suggest that NF-κB is at least partially involved in the IL-1β-mediated action on MIP-1α and -1β in NT2-N cells. IL-1β-mediated up-regulation of β-chemokine expression may have important implications in the immunopathogenesis of inflammatory diseases in the CNS.

AB - Chemokines are important mediators in immune responses and inflammatory processes of neuroimmunologic and infectious diseases. Although chemokines are expressed predominantly by cells of the immune system, neurons also express chemokines and chemokine receptors. We report herein that human neuronal cells (NT2-N) produce macrophage inflammatory protein-1α and -1β (MIP-1α and MIP-1β), which could be enhanced by interleukin (IL)-1β at both mRNA and protein levels. The addition of supernatants from human peripheral blood monocyte-derived macrophage (MDM) cultures Induced MIP-1β mRNA expression in NT2-N cells. Anti-IL-1β antibody removed most, but not all, of the MDM culture supernatant-induced MIP-1β mRNA expression in NT2-N cells, suggesting that IL-1β in the MDM culture supernatants is a major factor in the induction of MIP-1β expression. Investigation of the mechanism(s) responsible for IL-1β-induced MIP-1α and -1β expression demonstrated that IL-1β activated nuclear factor kappa B (NF-κB) promoter-directed luciferase activity in NT2-N cells. Caffeic acid phenethyl ester, a potent and specific inhibitor of activation of NF-κB, not only blocked IL-1β-induced activation of the NF-κB promoter but also decreased IL-1β-induced MIP-1α and -1β expression in NT2-N cells. These data suggest that NF-κB is at least partially involved in the IL-1β-mediated action on MIP-1α and -1β in NT2-N cells. IL-1β-mediated up-regulation of β-chemokine expression may have important implications in the immunopathogenesis of inflammatory diseases in the CNS.

KW - β-chemokines

KW - Interleukin-1β

KW - Macrophage inflammatory protein-1α

KW - Macrophage inflammatory protein-1β

KW - NT2-N

KW - Nuclear factor-κB

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