An immunoglobulin agent (IVIG) inhibits NF-kappaB activation in cultured endothelial cells of coronary arteries in vitro.
|Inflamm Res. 2004 Jun;53(6):253-6. Epub 2004 May 12.|
Ichiyama T, Ueno Y, Isumi H, Niimi A, Matsubara T, Furukawa S.
Department of Pediatrics, Yamaguchi University School of Medicine, 1-1-1 Minami-kogushi, Ube, Yamaguchi 755-8505, Japan. email@example.com
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-kappaB, 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-kappaB activation induced by TNF-alpha was evaluated by Western blot analysis and ELISA. Moreover, the inhibitory effects of IVIG on IkappaBalpha 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-kappaB activation induced by TNF-alpha in CAEC. Moreover, IVIG inhibited IkappaBalpha degradation, IL-6 production, and E-selectin expression induced by TNF-alpha in CAEC. CONCLUSION: The data suggest that IVIG inhibits NF-kappaB activation induced by TNF-alpha in CAEC, thereby possibly modulating IL-6 production and E-selectin expression.
PMID: 15167972 [PubMed - in process]