Abstract
Intensive use of corticosteroids may be accompanied by increased susceptibility to infections; hence, we investigated the effects of dexamethasone on the expression of antimicrobial peptides, termed human beta-defensins (hBD), by cultured bronchial epithelial cells and mononuclear phagocytes. The results revealed that dexamethasone inhibited the (stimulated) expression of mRNA for hBD-3, but not hBD-1 and hBD-2 by these epithelial cells. Dexamethasone did not affect the (stimulated) mRNA expression of hBD-1 and hBD-2 by mononuclear phagocytes, whereas these cells did not express hBD-3 mRNA.
Copyright 2001 Academic Press.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adrenal Cortex Hormones / pharmacology*
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Bronchi / cytology
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Cells, Cultured
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Dexamethasone / pharmacology
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Epithelial Cells / drug effects
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Epithelial Cells / metabolism
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Epithelial Cells / microbiology
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Gene Expression Regulation / drug effects*
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Humans
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Interferon-gamma / pharmacology
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Interleukin-8 / metabolism
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Lipopolysaccharides / pharmacology
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Macrophages / drug effects
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Macrophages / metabolism
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Monocytes / drug effects
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Monocytes / metabolism
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Pseudomonas aeruginosa / physiology
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Streptococcus pneumoniae / physiology
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Tumor Necrosis Factor-alpha / metabolism
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beta-Defensins / genetics*
Substances
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Adrenal Cortex Hormones
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DEFB1 protein, human
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DEFB4A protein, human
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Interleukin-8
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Lipopolysaccharides
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RNA, Messenger
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Tumor Necrosis Factor-alpha
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beta-Defensins
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Dexamethasone
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Interferon-gamma