Abstract
The chemokine RANTES is a potent chemoattractant for eosinophils. RANTES is produced by lung epithelial cells during eosinophil-rich inflammatory diseases such as asthma. In this study, we examined the effects of thiazolidinediones (TZD) on RANTES expression in a human lung epithelial cell line, A549. In A549 cells, interleukin-1beta and tumor necrosis factor-alpha induced endogenous RANTES protein secretion, mRNA expression, and promoter activity. The TZD inhibited these effects. Our data indicate that the suppression of the expression of RANTES can be accomplished by TZD treatment, raising the possibility that TZD might be of therapeutic value in diseases such as asthma.
MeSH terms
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Cell Line
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Chemokine CCL5 / biosynthesis
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Chemokine CCL5 / genetics*
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Chemotaxis, Leukocyte / drug effects
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Dexamethasone / pharmacology
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Eosinophils / drug effects
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Eosinophils / physiology*
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Epithelial Cells / drug effects
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Epithelial Cells / metabolism*
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Gene Expression Regulation / drug effects*
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Humans
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Hypersensitivity / blood
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In Vitro Techniques
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Interleukin-1 / pharmacology
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Luciferases / genetics
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Lung / drug effects
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Lung / metabolism
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Promoter Regions, Genetic / drug effects
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Pyrimidines / pharmacology
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RNA, Messenger / genetics
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Recombinant Proteins / biosynthesis
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Thiazoles / pharmacology*
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Thiazolidinediones*
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Transcription, Genetic / drug effects
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Transfection
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Tumor Necrosis Factor-alpha / pharmacology
Substances
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Chemokine CCL5
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Interleukin-1
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Pyrimidines
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RNA, Messenger
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Recombinant Proteins
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Thiazoles
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Thiazolidinediones
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Tumor Necrosis Factor-alpha
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Dexamethasone
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pirinixic acid
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2,4-thiazolidinedione
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Luciferases