Dexamethasone inhibits ozone-induced gene expression of macrophage inflammatory protein-2 in rat lung

To address the potential role of the chemokine macrophage inflammatory protein-2 (MIP-2) in airway inflammation, we examined whether MIP-2 may play a role in ozone-induced neutrophilic inflammation of airways and its modulation by dexamethasone in rat lung. Following ozone exposure, MIP-2 mRNA expre...

Full description

Saved in:
Bibliographic Details
Published in:FEBS letters 1995-04, Vol.363 (3), p.285-288
Main Authors: Haddad, E.-B., Salmon, M., Sun, J., Liu, S., Das, A., Adcock, I., Barnes, P.J., Chung, K.F.
Format: Article
Language:English
Subjects:
Animals
Base Sequence
Chemokine CXCL2
Cytokines - genetics
Dexamethasone
Dexamethasone - pharmacology
DNA Primers - chemistry
Gene Expression - drug effects
Inflammation
MIP-2 mRNA
Molecular Sequence Data
Monokines - genetics
Northern blot
Ozone
Ozone - pharmacology
Rat lung
Rats
Rats, Inbred BN
RNA, Messenger - genetics
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:To address the potential role of the chemokine macrophage inflammatory protein-2 (MIP-2) in airway inflammation, we examined whether MIP-2 may play a role in ozone-induced neutrophilic inflammation of airways and its modulation by dexamethasone in rat lung. Following ozone exposure, MIP-2 mRNA expression in the lung peaked at 2 h after exposure and slowly declined thereafter. Dexamethasone suppressed ozone-induced MIP-2 mRNA expression and neutrophil accumulation in the lung. We suggest that the MIP-2 mRNA induction may switch on the neutrophilic influx observed in this model of lung inflammation. Furthermore, the MIP-2 expression is regulated by dexamethasone which may represent one of the mechanisms by which glucocorticoids exert their potent anti-inflammatory properties.
ISSN:0014-5793
1873-3468
DOI:10.1016/0014-5793(95)00333-5