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

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- alpha (TNF- alpha ) is responsible for the patho...

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Bibliographic Details
Published in:Inflammation research 2004-06, Vol.53 (6), p.253-256
Main Authors: Ichiyama, T, Ueno, Y, Isumi, H, Niimi, A, Matsubara, T, Furukawa, S
Format: Article
Language:English
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Summary: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- alpha (TNF- alpha ) is responsible for the pathogenesis of acute KD. We examined whether or not IVIG inhibits TNF- alpha -induced activation of transcription factor NF- Kappa B, 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- Kappa B activation induced by TNF- alpha was evaluated by Western blot analysis and ELISA. Moreover, the inhibitory effects of IVIG on I Kappa B alpha degradation, interleukin-6 (IL-6) production, and E-selectin expression induced by TNF- alpha were evaluated by Western blot analysis, ELISA, and flow cytometry, respectively. Results: Western blot analysis and ELISA demonstrated that IVIG inhibits NF- Kappa B activation induced by TNF- alpha in CAEC. Moreover, IVIG inhibited I Kappa B alpha degradation, IL-6 production, and E-selectin expression induced by TNF- alpha in CAEC. Conclusion: The data suggest that IVIG inhibits NF- Kappa B activation induced by TNF- alpha in CAEC, thereby possibly modulating IL-6 production and E-selectin expression.
ISSN:1023-3830
DOI:10.1007/s00011-004-1255-3