Abstract
We determined in rat lung whether ozone exposure was associated with the expression of the chemokine, cytokine-induced neutrophil chemoattractant (CINC), and of the transcription factor, NF-kappa B. CINC mRNA expression peaked at 2 h after cessation of ozone exposure, and returned to basal levels by 24 h. DNA-binding activity of NF-kappa B showed a marked increase after ozone, maximal at 2 h. Dexamethasone inhibited CINC mRNA and NF-kappa B expression, together with neutrophilic inflammation. Our data supports the concept that ozone leads to NF-kappa B activation which increases CINC mRNA expression. These series of events could lead to neutrophilic inflammation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anti-Inflammatory Agents / pharmacology*
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Base Sequence
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Chemokines / metabolism*
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Chemokines, CXC*
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Chemotactic Factors / chemistry
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Chemotactic Factors / metabolism*
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Dexamethasone / pharmacology*
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Growth Inhibitors / chemistry
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Growth Inhibitors / metabolism*
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Growth Substances / chemistry
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Growth Substances / metabolism*
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Inflammation
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Intercellular Signaling Peptides and Proteins*
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Lung / metabolism*
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Molecular Sequence Data
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NF-kappa B / metabolism*
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Ozone / antagonists & inhibitors*
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Ozone / pharmacology
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RNA, Messenger / analysis
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Rats
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Rats, Inbred BN
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Specific Pathogen-Free Organisms
Substances
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Anti-Inflammatory Agents
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Chemokines
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Chemokines, CXC
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Chemotactic Factors
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Growth Inhibitors
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Growth Substances
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Intercellular Signaling Peptides and Proteins
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NF-kappa B
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RNA, Messenger
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Ozone
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Dexamethasone