UMMS Affiliation
Department of Pediatrics
Date
12-2003
Document Type
Article
Medical Subject Headings
Biological Markers; Butyric Acid; Carrier Proteins; Cell Differentiation; Cell Lineage; Clone Cells; Enzyme Activation; Eosinophils; Erythropoietin; Gene Expression Regulation; HL-60 Cells; Humans; Interferon-gamma; Interleukin-5; Maltose-Binding Proteins; Membrane Glycoproteins; NADPH Oxidase; Peroxidase; Tumor Necrosis Factor-alpha
Disciplines
Hematology | Oncology | Pediatrics
Abstract
The aim of this study was to investigate the effect of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) on NADPH oxidase activity and gp91-phox gene expression in HL-60 clone 15 cells as they differentiate along the eosinophilic lineage. The results were compared to the eosoniphilic inducers interleukin-5 (IL-5) and butyric acid. IFN-gamma (100 U/ml) and TNF-alpha (1000 U/ml) or IL-5 (200 pM) caused a significant increase in the expression of the eosinophil peroxidase (EPO) and the major basic protein (MBP) genes. Similar results were observed when the cells were cultured with 0.5 mM butyric acid for 5 days. IFN-gamma (100 U/ml) and TNF-alpha (1000 U/ml) also caused a significant increase in superoxide release by HL-60 clone 15 cells after 2 days compared with control or with butyric acid-induced cells. After 5 days, these cytokines and butyric acid induced an even stronger release of superoxide. HL-60 clone 15 cells cultured with IFN-gamma and TNF-alpha for 2 days showed a significant increase in gp91-phox gene expression. We conclude that IFN-gamma and TNF-alpha are sufficient to induce the differentiation of HL-60 clone 15 cells to the eosinophilic lineage and to upregulate gp91-phox gene expression and activity of the NADPH oxidase system.
Comments
Citation: J Interferon Cytokine Res. 2003 Dec;23(12):737-44. doi 10.1089/107999003772084851. Link to article on publisher's website
This is a copy of an article published in the Journal of Interferon & Cytokine Research © 2003 copyright Mary Ann Liebert, Inc. and available online at: http://online.liebertpub.com.