Inflammation Research

, Volume 53, Issue 6, pp 253–256

An immunoglobulin agent (IVIG) inhibits NF-κB activation in cultured endothelial cells of coronary arteries in vitro

Authors

    • Department of PediatricsYamaguchi University School of Medicine
  • Y. Ueno
    • Department of PediatricsYamaguchi University School of Medicine
  • H. Isumi
    • Department of PediatricsYamaguchi University School of Medicine
  • A. Niimi
    • Bayer Yakuhin Ltd.
  • T. Matsubara
    • Department of PediatricsYamaguchi University School of Medicine
  • S. Furukawa
    • Department of PediatricsYamaguchi University School of Medicine
Original Paper

DOI: 10.1007/s00011-004-1255-3

Cite this article as:
Ichiyama, T., Ueno, Y., Isumi, H. et al. Inflamm. res. (2004) 53: 253. doi:10.1007/s00011-004-1255-3

Abstract

Objective:Kawasaki disease (KD) is an acute febrile vasculitis of unknown etiology that may lead to cardiovascular disorders. High-dose intravenous immunoglobulin (IVIG) therapy is well established as a standard therapy for KD. Tumor necrosis factor-α (TNF-α) is responsible for the pathogenesis of acute KD. We examined whether or not IVIG inhibits TNF-α-induced activation of transcription factor NF-κB, a factor that is essential for the expression of proinflammatory cytokines, in human coronary artery endothelial cells (CAEC).

Methods:The inhibitory effect of IVIG on NF-κB activation induced by TNF-α was evaluated by Western blot analysis and ELISA. Moreover, the inhibitory effects of IVIG on IκBα degradation, interleukin-6 (IL-6) production, and E-selectin expression induced by TNF-α were evaluated by Western blot analysis, ELISA, and flow cytometry, respectively.

Results:Western blot analysis and ELISA demonstrated that IVIG inhibits NF-κB activation induced by TNF-α in CAEC. Moreover, IVIG inhibited IκBα degradation, IL-6 production, and E-selectin expression induced by TNF-α in CAEC.

Conclusions:The data suggest that IVIG inhibits NF-κB activation induced by TNF-α in CAEC, thereby possibly modulating IL-6 production and E-selectin expression.

Coronary artery endothelial cells E-Selectin Interleukin-6 Intravenous immunoglobulin NF-κB

Copyright information

© Birkhäuser-Verlag Basel 2004